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Cardiovascular

phase 2 test 7 (revised)

QuestionAnswer
aneurysm localized dilation of the wall of a blood vessel
angina pectoris paroxysmal thoracic chest pain, pressure, and choking feeling caused by decreased O2 to the myocardium
arteriosclerosis arterial disorder characterized by loss of elasticity, thickening, and calcification of the arterial walls
artherosclerosis arterial disorder characterized by yellowish plaques of cholesterol, lipids, and cellular debris in the inner layers of the walls of arteries
bradycardia slow heart rhythm characterized by a pulse less than 60 beats per minute (bpm)
cardioversion restoration of the heart's normal sinus rhythm by delivery of a synchronized electric shock through 2 paddles placed on the patient's chest
coronary artery disease (CAD) conditions that obstruct blood flow in the coronary arteries
defibrillation converting ventricular fibrillation by delivering a direct electrical counter shock to the pericardium
dysrhythmia an abnormal cardiac rhythm; also call an arrhythmia
embolus a foreign object, blood clot, fat, air or amniotic fluid in the bloodstream that becomes lodged in a blood vessel
endarterectomy surgical removal of the intimal lining of an artery
heart failure syndrome of circulatory congestion due to the heart's inability to act as an effective pump
hypoxemia abnormal deficiency of oxygen in the arterial blood
intermittent claudication weakness of the legs accompanied by cramp-like pain in the calves caused by decreased arterial blood circulation to the leg muscles
ischemia decreased blood supply to a body organ or part; often marked by pain and organ dysfunction
myocardial infarction (MI) necrosis of a portion of the cardiac muscle caused by an occlusion of a major coronary artery or one of its branches
occlusion obstruction or closing off in a canal, vessel, or passage of the body
orthopnea patient must sit-up or stand to breathe deeply and comfortably
peripheral pertaining to the outside, surface or surrounding area
pleural effusion an accumulation o fluid in the thoracic cavity between the visceral and parietal layers
polycythemia an abnormal increase in the number of red blood cells in the blood
pulmonary edema acculumulation of extravascular fluid in lung tissues and alveoli; most commonly caused by left-sided heart failure
tachycardia heart rate of greater than 100 bpm
where the heart lies mediastinal space
lower border of heart called apex
upper border of heart called base
layers or heart wall (outter to inner) pericardium myocardium endocardium
pericardium 2 part membrane that comprises the outside layer of the heart
myocardium constructed of cardiac muscle
endocardium lines the inner surface of the heart
right atrium uppper right chamber; receives deoxygenated blood from body via vena cava, and from the heart via the coronary sinus
right ventricle lower right chamber; receives blood from the right atrium through the tricuspid valve, pumps blood to the lungs through the pulmonic valve via the pulmonary arteries
left atrium upper left chamber; receives oxygenated blood from the lungs via the pulmonary veins
left ventricle lower left chamber; receives blood from the left atrium through the mitral valve, most muscular section of heart, pumps oxygenated blood through aortic valve to all parts of body
arteries carrying blood away from heart
capillaries tiny blood vessels joining arterioles & veinoles
veins vessels that carry blood to the heart
coronary circulation right & left coronary arteries (RCA & LCA) branch off from the aorta, just above the aortic valve, encircle the heart like a crown, perfuse the myocardium with the needed O2 & nutrients
RCA perfuses the RA, RV, and the posterior portion of the LV
LCA perfuses anterior and lateral wall of the LV, the apex of the LV and the LA
blood containing CO2 & waste products flows into coronary veins to coronary sinus, which finally empties into the RA
systemic circulation circulates blood from the left ventricle to all parts of the body & back to the right atrium; carries O2 & nutrients to all body tissues & removes products of metabolism
pulmonary circulation circulates blood from the right ventricle to the lungs & back to the left atrium of the heart; carries deoxygenated blood to the lungs to be re-oxygenated & removes the metabolic waste product, carbon dioxide
automaticity inherent ability of the heart muscle tissue to contract in a rhythmic pattern
irritability the ability of the heart muscle tissue to respond to a stimulus
sinatrial (SA) node located in the superior portion of the RA, pacemaker of the heart, causes contraction of the atria
atrioventricular (AV) node located in the base of the RA, there is a short delay in the transmission of impulses at the AV node, the delay of the impulse by the AV node allows the right & left atrium to complete contraction & assist the ventricles to fill
bundle of his (AV bundle) located in the inter-ventricular septum with branches extending to all parts of the ventricle walls, divides into left & right bundle branches which divide into Purkinje Fibers, then surround the ventricles and cause contraction of the ventricles
complete heartbeat atria contract while ventricles relax ventricles contract while atria relax complete diastole & systole of borth constitute a cardiac cycle
systole phase of contraction, begins with closure of the mitral & tricuspid valves, produces the "lubb"
diastole phase of relaxation, begins with closure of pulmonic & aortic valves, produces the "dubb" (S2)
chest radiograph illustrates heart size, shape, and position outline of shadows & lung abnormalities are also shown
fluoroscopy motion radiograph, aloows observatoin of movement
angiogram series of radiograph taken after injection of radiopaque dye into an artery helpful in Dx of occlusion, aneurysm, and other congenital arterial abnormalities
cardiac catheterization used to visualize the heart, great vessels, & coronary arteries
uses of cardiac catheterization Dx of cardiac pathology measure pressures within the heart cardiac competence valvular defects iodine base contrast dye may be used to allow better visualization of coronary blockage
cardiac catheterization performed under steile conditions requires informed consent catheter is passed through a peripheral vessel to the heart patient remains supine for a designated period of time post-procedure pressure is applied over the insertion site iodine allergy?
electrocardiogram (ECG/EKG) graphic study of the electrical activities of the myocardium
ambulatory ECG or Halter monitor used for outpatient monitoring, for patients with cardiac disease & normal ECG, patient keeps diary of symptoms during movement
heart monitor used to continually monitor electrical activity of patients who have dysrhythmias
exercise/stress test conducted in a lab setting, used to test cardiac function during exertion
thallium scanning radioisotope injected intravenously to assess circulation using a scanning camera; usually combined with stress test
echocardiography ultrasound directed at the heart & is used to show size, shape, motion, and ejection fraction (cardiac output)
CBC WBC, differential, PLT, Hgb, & Hct
coagulation stiudies used to monitor patients receiving anticoagulation drug therapy
serum cardiac markers (cardiac enzymes) proteins released in blood due to necrotic heart muscles after and MI (CK, CK-MB, & troponin 1)
which cardiac marker most specific & considered the gold standard? toponin 1
T/F arteriosclerosis & atherosclerois accompany the aging process true
what comprise plaque deposits? cholesterol, lipids, cellular debris
what happens with plaque buildup? narrows the lumen of arteries, reduces blood volume to area
how is the severity of CAD measured? degree of obstruction & number of vessels involved
when do symptoms of CAD develop? 75-80% obstruction of coronary blood flow to the myocardium
non-modifiable risk factors for CAD family history age gender ethnicity
modifiable risk factors for CAD smoking, hyperlipidemia, hypertension, physical activity, stress, obesity, diabetes
how are symptoms of angina pectoris perceived by patient chest pain or discomfort
T/F angina pectoris leads to cellular necrosis false
what can cause angina pectoris? any factor that causes an imbalance between demand & supply of blood flow to the myocardium
factors that increase cardiac workload hypertension, stress, temperature extremes, exercise, smoking, atherosclerosis
unstable angina unpredicatable & transient episode of severe & prolonged discomfort that at rest has never been experienced before or considerably worse than the previous episode
how long angina attacks last 3-5 minutes
other symptoms of angina pectoris dyspnea, pallor, diaphoresis, faintness, palpitations, dizziness
retrosternal behind the sternum
substernal below the sternum
precordial around the heart or epigastric area
t/f angina pectoris pain may radiate to left shoulder & arm true
tests to differentiate angina from myocardial infarction cardiac enzymes, EKG, stress tests, cardiac catheterization
3 major types of medications used for treatment of angina pectoris vasodilators, beta-blockers, calcium channel blockers
additional medications for angina pectoris supplemental O2, aspirin
indications for antianginal agents treat & prevent attacks ONLY nitrates may be used for acute attacks beta blockers & calcium channel blockers
action of antianginal agents increase coronary blood flow by dilating coronary arteries & improving collateral flow to ischemic regions, produce vasodilation, decrease left ventricular end-diastolic pressure & volume
therapeutic effects of antianginal agents relief & prevention of anginal attacks
examples of antianginal agents nitroglycerin
side effects of antianginal agents dizziness, headache, hypotension, tachycardia, syncope, nausea, vomiting, flushing, tolerance
surgical interventions used to treat angina pectoris CABG, PTCA, stent placement
coronary artery bypass graft vein grafts are sewn to the heart by passing the blocked coronary artery
percutaneous transluminal coronary angioplasty balloon-tipped catheter is passed into a blocked artery and then inflated pressing the plaque against the coronary wall
stent placement used to treat abrupt or threatened vessel closure following PTCA
nursing interventions for angina pectoris promoting comfort, tissue perfusion, activity & rest, feeling of well being & relief of anxiety; teach that patient must seek medical attention if pain doesn't subside in 15 minutes
cellular damage & necrosis to myocardium from ischemia occurs after 35-45 minutes
MI clinical manifestations similar to that of angina but usually more severe & is unrelieved by nitroglycerin tablets
MI angina symptoms longer duration, squeezing/crushing, not relieved by rest
MI signs & symptoms gray facial color, cold & diaphoretic, weak thready tachycardia bradycardia, oliguria secondary to decreased cardiac output, elevated temperature from destruction of myocardial tissue
medical management of myocardial infarction primary goal to prevent further tissue damage & limit the size of the infarction, facilitate cardiac tissue perfusion & reducing the workload of the heart
pharmacological management of MI analgesics, vasodilators, tranquilizers, anticoagulants, antiarrhythmic, O2 therapy, stool softeners, thrombolytic agents
inefficient circulation leads to the congestion of body organs with blood & tissue fluid
heart failure is thought of as a ________ problem neuro hormonal
progression of HF is a result of chronic release of _____________ catecholamines
what hormones fall under catecholamines epinephrine & norepinephrine
renin-angiotensin-aldosterone system renin activates angiotension I formation - ACE converts angiotension 1 to angiotension 2 (potent vasoconstrictor) - 2 induces aldosterone secretion from the adrenal gland (Na & H2O) - increased BP
causes of CHF congenital defects, artherosclerosis, arteriosclerosis, MI, DM, HTN, valvular heart disease
conditions that increase cardiac output infection, stress, hyperthyroidism, pregnancy, anemia
clinical manifestations of HF decreased cardiac output, left ventricular failure, right sided failure
left ventricular failure increased pressure in the left side of the heart backs up to the pulmonary system & lungs become filled with fluid, inability of left ventricle to effectively pump enough blood to meet needs of body tissues
signs & symproms of left ventricular failure decreased cardiac output, pulmonary congestion, cough, dyspnea, orthopnea, frothy blood tinged sputum, pulmonary crackles
which ventricle often first affected by coronary atherosclerosis and HTN? left
right ventricular failure inability of right ventricle to effectively pump enough to meet the needs of body tissues because of increased pressure in the pulmonary circulation results in edema in extremities & various body organs
right ventricular failure most often caused by ________ left-sided failure
signs & symptoms of right ventricular failure nocturia, organ dysfunction, ascites, weight gain, JVD
diagnosis of CHF made by presenting signs & symptoms, pt history, diagnostic/laboratory tests
diagnostic tests of CHF chest x-ray, ECG, echocardiography, exercise stress testing, cardiac catheterization, ABG, LFT, serum electrolytes & enzymes
medical management of HF goal is to reduce workload of heart & improve pumping ability, digitalis, diuretics, nitrates, ACE inhibitors, limiting activity, low Na diet, fluid restriction, paracentesis, O2 therapy
pitting edema increased in interstitial fluid & appears i ndependent areas of body
nursing interventions for heart failure prevent disease progression, and complications and maintain ADLs
pulmonary edema complication of left sided heart failure
clinical manifestations of pulmonary edema respiratory distress, frothy sputum, blood tinged, restlessness, agitation, disorientation, diaphoresis, dyspnea, tachypnea,tachycardia, pallor, cyanosis, cough, wheezes,crackles,cold extremities
diagnostic tests for pulmonary edema physical exam, chest x-ray, ABG sampling
medical management for pulmonary edema improve oxygenation, cardiac output, reduce pulmonary congestion, place pt in high-Fowler's, MSO4 titrate IV, nitro, diuretics, inotropic agents, nitroprusside
action of inotropic agents stimulates B1 (myocardial) adrenergic receptors with relatively minor effect on heart rate or peripheral blood vessels, increased cardiac output, BP & improved renal blood flow
indications for inotropic agents dobutamine (dobutrex): inotropic support in CHF, cardiogenic shock dopamine (inotropin): hypotension associated with shock, renal insufficiency
category of inotropic agents therapeutic: inotropics pharmacologic: adrenergics agonist
contraindications of inotropic agents pupil dilation (mydriasis) narrow-angle glaucoma hypersensitivity to bisulfites (some prodcuts)
precautions of inotropic agents hypvolemia, MI, occlusive vascular diseases, pregnancy or lactation, children
side effects of inotropic agents headache, SOB, hypertension, increased HR, premature ventricular contractions, agina pectoris, arrhythmias, hypotension, palpitations, N/V, phlebitis, hypersensitivity reactions
interactions of inotropic agents beta blockers may negate the effect of dobutamine, increased risk of arrhythmias/hypertension with some anesthetics, MAO inhibitors, oxytocics, or tricyclic antidepressants
nursing implications of inotropic agents monitor BP, HR, ECG, pulmonary capillary wedge pressure, cardiac output, CVP, urinary output consult physician for parameters may cause hypokalemia monitor electrolytes, BUN, creatinine, PT IV meds potentially dangerous
toxicity & overdose of inotropic agents phentolamine for extravasation
2 primary pathologies of valvular heart disease stenosis insufficiency
primary cause of valvular heart disease in children congenital defects
primary cause of valvular heart disease in adults rheumatic heart disease
_____ & ______ valves affected most frequently in valvular disease due to greater workload & blood volume on the left vs right side of heart mitral & aortic
4 valvular heart disorders mitral stenosis & insufficiency, aortic stenosis & insufficiency, tricuspid stenosis & insufficiency, pulmonary stenosis & insufficiency
signs & symptoms of valvular heart disease related to decreased cardiac output
diagnostic tests to confirm valvular heart disease chest x-ray, echocardiogram, cardiac catheterization
medical management for valvular heart disease activity limitations, Na restricted diet, diuretics, digoxin, antidysrhythmics, anticoagulants, antibiotics
surgical intervention for valvular heart disease indicated lifestyle affected, medical therapy no longer alleviates symptoms, diagnostic evidence of progressive myocardial failure
common valves used for valve replacement surgery porcine (pig), heterograft (taken from another species), homograft, ball in cage, mechanical
use of anticoagulant agents prevent & treat thromboembolic disorders including DVT, PE, A-fib with embolization management of MI sequentially or in combination with thrombolytics and/or antiplatelet agents
action of anticoagulant agents prevent clot extension & formation potentiates the inhibitory effect of antithrombin on fact Xa & thrombin
T/F anticoagulants dissolve clots false
another name for anticoagulants antithrombotic
examples of anticoagulants heparin, warfarin, LMWHs, direct thrombin inhibitors, selective factor Xa inhibitor
contraindications of anticoagulants hypersensitivity, underlying coagulation disorders, ulcer disease, malignancy, recent surgery, active major bleeding, pregnancy, epidural catheter (LMWHs contraindicated but can be given 2 hours after removal)
main complication of anticoagulants bleeding
labs to monitor for anticoagulant therapy CBC, platelet count, stools for occult blood, PT & INR for warfarin, PTT for heparin therapy, H & H, bleeding time
antidote for heparin & LMWH overdose protamine sulfate
antidote for warfarin overdose vitamin K
patients on anticoagulant therapy should not take ____, ____, ____ without consulting health care professional aspirin, naproxen, ibuprofen
why would a patient be prescribed warfarin in addition to a heparin infusion? heparin often used to initiate therapy with oral anticoagulants are prescribed until lab tests indicate an adequate therapeutic response
nursing diagnoses for valvular heart disease activity intolerance fluid volume excess
cause of rheumatic heart disease rheumatic fever
what happens to tissue affected by rheumatic fever becomes necrotic and leaves scar tissue
most common site affected by rheumatic heart disease the valves
clinical manifestations of rheumatic heart disease specific to valve involved generalized: increased pulse, epistaxis, anemia, joint involvement , nodules found on joints & SQ tissues
commissurotomy surgical procedure performed to open a stenotic (narrowed)valve. scalpel incision weides the valve
subjective assessment for rheumatic heart disease joint pain (polyarthritis), abdominal pain, lethargy, fatigue
objective assessment for rheumatic heart disease skin: erythema marginatum (wavy lines of trunk that disappear rapidly), small erythmatous circles,involuntary purposeless movement (Sydenham's Chorea), heart murmur (hallmark sign)
diagnostic tests for rheumatic heart disease echocardiogram, EKG, lab values
medical management for rheumatic heart disease prevention more effective, rapid & prolonged treatment of group A strep pharyngitis with PCN, carditis present: BR until HF is controlled, NSAIDs, well balanced diet, valve replacement, commissurotomy
nursing interventions for rheumatic heart disease minimizing joint pain, maintain BR for pts with carditis
patient teaching for rheumatic heart disease understanding of disease process, prophylactic antibiotic therapy, optimal nutrition
pericarditis inflammation of the pericardium, the membranous sac enveloping the heart
causes of pericarditis acute or chronic, bacterial, viral, & fungal chest trauma MI especially common after thoracic surgery Hodgkin's breast cancer lung cancer renal failure (azotemia) SLE radiation meds
clinical manifestations of pericarditis debilitating pain often mimicking the pain of an MI, pericardial friction rub, grating, scratching, leathery sounds, cardiac tamponade, decreased CO, death
if fluid in pericardial space sufficient to compress heart, ____ _____ occurs pulsus paradoxus
subjective assessment for pericarditis anxiety, malaise, dyspnea, muscle aches, excruciating precordial pain
objective assessment for pericarditis pericardial friction rub, heart sounds distant and muffled, elevated temperature, nonproductive cough, rapid forcible pulse, rapid shallow breathing
diagnostic tests for pericarditis chest x-ray, EKG, echocardiography, leukocytosis, elevated sedimentation rate
medical management for pericarditis analgesia, O2, parenteral fluids, NSAIDS, corticosteroids, pericardiocentesis (pericardial tap), pericardial fenestration (pericardial window)
nursing interventions for pericarditis reduce anxiety, position to help relieve chest pain, immediately report signs of inadequate CO, reinforce information provided by physician, baseline vitals, measure and fluid obtained, reinforce dressings as ordered, monitor R/P/BP/rhythm
endocarditis infection or inflammation of the inner layer of heart tissue, particularly the heart valves
causes of endocarditis after cardiac surgery, infection, intrusive procedures, IV drug abuse
subjective data of endocarditis often has insidious onset, recurrent fever, flu-like symptoms, HA, undue fatigue, joint pain, chills, chest pain
how symptoms of endocarditis can change abruptly emobolization or heart failure occurs
objective data for endocarditis purplish painful nodules on fads of fingers & nose, black longitudinal line in nails, new heart murmur, petechiae in conjunctiva mouth & legs, weight loss
diagnostic findings in endocarditis leukocytosis, blood cultures, transesophageal echocardiography, EKG
medical management for endocarditis goal: decrease workload of heart IV antibiotics, transitioning to outpatient treatment, prophylaxis antibiotics, valve replacement
nursing interventions for endocarditis based on S&S, promoting rest & comfort, monitor culture & sensitivity, antibiotics, weight, pulse, rhythm, prevent nosocomial infections, relieve activity intolerance
myocarditis inflammation of the myocardium or the muscle layer of the heart
causes of myocarditis viral, bacterial, fungal, endocarditis, pericarditis, idiopathic
signs & symptoms of myocarditis often vague, vary depending on site of infection cardiac enlargement, murmur, gallup, tachycardia, dysrhythmias
medical management of myocarditis BR, O2, antibiotics, antinflammatory
nursing interventions for myocarditis monitor all subjective/objective data, monitor for cardiomyopathy
nursing diagnoses for carditis decreased cardiac output, pain, fluid volume excess
major indications for cardiac transplant severe weakness of cardiac muscle (cardiomyopathy): 50% of all transplants end stage inoperable CAD: 40% transplants
contraindications for cardiac transplant systemic disease with poor prognosis active infection
factors considered prior to patient receiving donor heart general condition of vital organs, age, emotional outlook, presence of other chronic diseases, availability of support systems
major goals of nursing interventions for cardiac transplants client understands: purpose, prep, procedures, post-op care infection-free cofident of provider's expertise realistic attitude physically & emotionally prepared for surgery
indication for immunosuppressant agent prevention of transplant rejection reactions, organ rejection, management of selected autoimmune diseases
immunosuppressants used with corticosteroids for prevention of transplantation rejection reactions azathiprine (Imuran) cyclosporine (Neoral, Sandimmune, Gengraf) mycophenolate (CellCept)
immunosuppressant used with corticosteroids for prevent organ rejection tacrolimus (Prograf/Protopic)
only drug indicated for reversal of organ rejection once it's started muromonab-CD3
immunosuppressants used for management of autoimmune disease azathioprine (Imuran) cyclophosphamide (Cytoxan, Neosar) methotrexate (amethopterin, Folex, Trexall)
action of immunosuppressant agents interferes with ability of immune system to repond to antigen stimulation by inhibiting cellular & humoral immunity suppress immune responses in certain disease states alter T-cell function monoclonal antibodies
contraindications of immunosuppressants hypersensitivity to drug or vehicle previous muromonab therapy, fluid volume overload, fever >100F
side effects/adverse reactions of immunosuppressants increased risk of infection, trembling or shaking of hands, anorexia, N/V, megaloblastic anemia, leukopenia, pancytopenia, thrombocytopenia
patients should avoid concurrent digestion of _______ or _______ & immunosuppressants because it increases absorption & should be avoided grapefruit grapefruit juice
nursing implications for immunosuppressants monitor for infection, unusual tiredness/weakness, fever/chills, frequent need to urinate, symptoms of organ rejection, daily nutritional status
side effects of immunosuppressants high fever & chills, headache, dizziness, malaise, tremor, N/V/D, ABD pain, chest pain, muscle & joint pain, generalized weakness, SOB, CRS, labs
effects of aging on inner walls of arteries become thick & less compliant
shock life-threatening response to alterations in circulation that results in inadequate delivery of oxygen to tissues & cells, & their subsequent dysfunction & death
when does shock begin when cardiovascular system fails
types of shock hypovolemic distributive obstructive cardiogenic
4 stages of shock initiation compensatory progressive refractory (irreversible)
types of fluids administered to patient with hypovolemic shock crystalloid, colloid, blood
priorities for caring for a patient with shock ABCs
shock involves one or more of blood volume decreases heart failure as an effective pump peripheral vessel dilation
causes of hypovolemic shock hemorrhage, V/D, burns, large draining wounds, reduced fluid intake, diaabetes insipidus, DKA
distributive shock adequate volume, inadequate perfusion vascular beds dilated insufficient blood flow
types of distributive shock neurogenic, septic, anaphylactic
causes of distributive-neurogenic shock injury/disease to upper SC spinal anesthesia vasodilators
normal blood pressure systolic <120 diastolic <80
prehypertension 120-139/80-89
hypertension pressures >140 and/or <90
atrial blood pressure determined by pressure exerted by blood on the vessel walls important factors: blood flow, peripheral vascular resistance
increased vascular resistance caused by vasoconstriction and/or narrowing of the lumen of the peripheral blood vessel
what controls vasoconstriciton & vasodilation sympathetic nervous system renin-aniotensin system
types of hypertension primary, secondary, malignant
primary hypertension essential, arteriolar changes, sympathetic nervous system activation, hormonal influence, RAAS stimulation
secondary hypertension attributed to an identifiable medical diagnosis renal vascular disease, adrenal cortex disease, primary aldosteronism, Cushing's syndrome, pheochromocytoma, coarctation of the aorta, head trauma, cranial tumor, pregnancy-induced
malignant hypertension severe rapidly progressing elevation in BP: diastolic >120 damages small arterioles in major organs, heart, kidneys, brain, eyes
most distinguishing feature of malignant hypertension inflammation of arterioles of eyes (arteriolitis)
malignant hypertension most common in black males under 40
clinical manifestations of HTN awakening with headache, blurred vision, spontaneous epistaxis
HTN diagnostic tests CBC, electrolytes, lipid profile, fasting blood glucose, creatinine, BUN, UA, chest radiograph, ECG, possible echo, IVP
why does HTN often go untreated usually asymptomatic until target organ damage begins
goal of HTN management older adults: 140/90 or below younger adults: 131/85 or below
drug therapy for HTN diuretics, beta blockers, ACE inhibitors, angiotensin II receptor blockers, calcium channel blockers, alpha-agonist
modifible risk factors of vascular disease smoking, HTN, HLD, obesity, lack of exercise, emotional stresss, DM
nonmodifible risk factors of vascular disease age, gender, family history
first symptom of decreased arterial circulation pain due to arterial insufficiency & ischemia
+1 on pulse scale barely palpable, intermittent
+2 on pulse scale weak and thready, but consistent quality and palpable
+3 on pulse scale normal strength & quality
+4 on pulse scale bounding easily palpable may be visible
assessment of venous system in vascular disease edema, changes in skin pigmentation, stasis ulcers, peripheral pulses absent, pain, aching, cramping-
PATCHES pulses, appearance, temp, cap refill, hardness, edema, sensation
noninvasive diagnostic tests for vascular disease treadmill, plethysmography, Doppler ultrasound, Duplex scanning
invasive diagnostic tests for vascular disease venography, I-gribrinogen uptake, angiography, D-dimer serum test, DSA
arteriosclerosis obliterans narrowing or occlusion of the intima and media blood vessel wall
clinical manifestations of arteriosclerosis obliterans pain, decreased/absent pulses, skin changes, 5 Ps
5 Ps of vascular disease pain, pallor, pulselessness, paresthesia, paralysis
prognosis for arteriosclerosis obliterans ischemia may lead to necrosis, ulceration, and gangrene
medical management of arteriosclerosis obliterans focused on preventing complete arterial occlusion, anticoagulants, heparin, warfarin, fibrinolytics/thrombolytics, vasodilators controversial
surgical interventions for arteriosclerosis obliterans embolectomy, endartectomy, percutaneous trnasluminal angioplasty
symptoms of arterial embolism severe pain, absent distal pulses, numbness/tingling/cramping, pallor, loss of sensation, tissue necrosis occurs unless obstuction is relieved
diagnostic tests for arterial embolism ultrasonography, angiography
medical management for arterial embolism heparin/warfarin, thrombolytics, endartectomy, embolectomy, thrombectomy
clinical manifestations of arterial aneurysm may be asymptomatic, large pulsating mass, embolization distal to aneurysm, effects are based on shape & site, experience feelings of doom, severe chest pain with rupture of AAA
diagnostic tests for arterial aneurysm fluoroscopy, chest radiograph, CT scan
medical management for arterial aneurysms monitor for complications, control HTN #1, surgical intervention
etiology & pathophysiology of Buerger's Disease (Thromboangiitis Obliterans) inflammation of blood vessels that's associated with formation of clots & fibrosis of blood vessel wall (primarily affects lower extremities)
clinical manifestations of Buerger's Disease inflammation of the vessel wall, instep claudication, symptoms are usually equal bilaterally, may occur at rest & be frequent & persistent, skin may be cold & pale, ulcferations, increased sensitivity to cold
diagnostic tests of Buerger's Disease arteriography, digital subtraction angiography, doppler ultrasound, exercise testing
medical management of buerger's disease prevent progression, smoking cessation, buerger-allen exercises to develop collateral circulation, care of ulcerations, amputation with gangrene
etiology of raynaud's disease underlying cause unknown, or may be secondary to another condition such as scleroderma, RA, SLE, drug intoxication, occupational trauma
clinical manifestations of raynaud's disease chronically cold hands & feet, pallor, coldness, numbness, cutaneous cyanosis, pain with spasms, chronic may result in ulcerations of fingers & toes
diagnostic tests for raynaud's disease cold stimulation test
medical management of raynaud's disease biofeedback tech, vasodilators, calcium channel blockers, vascular smooth muscle relaxants, sympathectomy, amputation
prognosis for raynaud's disease can be controlled by protection from the cold, attacks may continue
factors that contribute to thrombophlebitis inactivity, trauma to vessel wall, venous stasis, hypercoagability, MI, HF, elderly patients, surgery that manipulates blood vessels, immobilization after surgery
clinical manifestations of thrombophlebitis size of calf or thigh may increase in circumference, pain on dorsiflexion (Homan's sign), erythema, warmth, tenderness
diagnostic tests for thrombophlebitis venous doppler, duplex scanning, venogram, d-dimer
medical management for thrombophlebitis bed rest, moist heat, elevation, anti-embolism stockings, NSAIDs, IV heparin, warfarin, LWMH, enoxaparin, dalteparin, thrombectomy, transvenous placement of grid, umbrella (Greenfield filter)
causes of varicose veins congenitally defective valves, incompetent valve, absent valve, external pressure on leg from pregnancy, poor posture, constrictive clothing, prolonged standing
diagnostic tests for varicose veins trendelenburg's test
medical management for varicose veins elastic stockings, rest periods, elevation, sclerotherapy, surgery
etiology of venous stasis ulcer deep vein insufficiency and stasis of the blood in the venous system
clinical manifestations of venous stasis ulcer pain, skin visibly ulcerated accompanied by dark pigmentation, edema, pedal pulses may be present
diagnostic tests for venous stasis ulcers doppler US, venography
medical management for venous stasis ulcers prevent infection, promote wound healing, diet, debridement, antibiotics, Unna's boot
use of antiplatelet agents prevent stroke in patients who have had a completed thrombotic stroke or precursors to stroke and are unable to tolerate aspirin
action of antiplatelet agents inhibits platelet aggregation, prolongs bleeding time
contraindications of antiplatelet agents hypersensitivity, bleeding disorders, active bleeding, severe liver disease
side effects of antiplatelet agents dizziness, headache, weakness, N/V/D, abnormal LFTs, anorexia, GI fullness, pain, rashes
interactions of antiplatelet agents aspirin potentiates the effect of ticlopidine on platelets, increase risk of bleeding with heparins/warfarin/throbolytic agents
toxicity and overdose of antiplatelet agents prolonged bleeding time is normalized within 2 hours after administration of IV methylprednisolone
how to implement antiplatelet agents PO: administer with food or immediately after eating to minimize GI discomfort & increase absorption
action of thrombolytic agents convert plasminogen to plasmin
therapeutic effects of thrombolytic agents lysis of thrombi in coronary arteries, lysis of pulmonary emboli or DVT
uses for thrombolytic agents actute MI, acute massive pulmonary emboli, acure ischemic stroke, occluded central venous access devices, acute DVT, acute arterial thrombi, occluded arteriovenous cannulae
contraindications of thrombolytic agents active internal bleeding, history of CVA, recent (within 2 months) intracranial or intraspinal injury or trauma, intracranial neoplasm, AV malformation, aneurysm, severe uncontrolled HTN, known bleeding tendencies, hypersensitivity
side effects of thrombolytic agents intracranial hemorrhage, epistaxis, gingival bleeding, bronchospasm, hemoptysis, hypotension, reperfusion, arrhythmias, GI bleeding, retroperitoneal bleeding, N/V, GU tract bleeding, ecchymoses, flushing, urticaria, bleeding, musculoskeletal pain, fever
in case of overdose of a thrombolytic agent, do NOT administer _________, it has antiplatelet activity dextran
antidote of thrombolytic agents aminocaproic acid (Amicar)
how does high blood pressure increase the workload of the heart? damages the arteries & causes an increased resistance of the arterioles to the flow of blood
prognosis of secondary HTN subsides when underlying condition corrected
drug therapy used to treat uncomplicated HTN diuretics, beta blockers, ACE inhibitors, angiotensin II receptor blockers, calcium channel blockers, alpha-agonist
special considerations when treating HTN DM, HF, MI, African-Americans
non-pharmacological management to treat HTN weight loss, reduced saturated fats, limit alcohol intake, exercise, reduce sodium intake, smoking cessation, relaxation techniques
side effects of antihypertensive agents headache, hypotension, bradycardia, tachycardia, N/V
antihypertensive agents may negate the therapeutic effectiveness of antihypertensives, antihistamines, NSAIDs, bronchodilators, decongestants, appetite suppressant, antidepressants, MAOI, hypokalemia increases risk of digoxin toxicity
conduction system of the heart controlled by autonomic nervous system - sympathetic, parasympathetic
2 characteristics of heart muscle automaticity, irritability
order of conduction through heart SA node - AV node - Bundle of His - Purkinje fibers
P wave represents depolarization of atria
QRS complex represents ventricular depolarization
PR interval represents time it takes an impulse to travel from SA node across the atria to the AV node fibers
T wave represents repolarization of the ventricle
ST segment represents early repolarization of the ventricular muscle
analysis of rhythm strip Rate: 60-100 bpm Rhythm: regular P wave: present for each QRS complex, identical PR interval: normal (0.12-0.20 sec) QRS complex: normal T wave: upright NSR
anaylsis of rhythm strip rate: >100 rhythm: regular P wave: present for each QRS, identical PR interval: normal QRS complex: normal T wave: normal sinus tachycardia
rate: <60 rhythm: RR, PP intervals regular P wave: present, normal, identical QRS: normal T wave: normal sinus bradycardia
rate: usually 150-250 rhythm: regular P wave: present, normal, identical PR interval: normal QRS: normal T wave: normal supraventricular tachycardia
AV block defect in the AV slows or impairs conduction
first degree AV block delayed conduction through the AV node causes prolonged PR interval
third degree AV block complete heart block, complete AV dissociation
PR interval: not measurable QRS: wide & bizarre T wave: usually deflected opposite the QRS premature ventricular contraction
rate: usually between 140-240 rhythm: usually regular P wave: not visible QRS: wide & bizarre T wave: usually deflected opposite to the QRS & difficult to see ventricular tachycardia
rate: unmeasurable rhythm: irregular P wave: not present QRS: not measurable (no definable complexes) T wave: not present ventricular fibrillation
seconda degree AV block type I consecutively prolonged PR interval until a QRS in dropped, more Ps than QRSs
second degree AV block type II P waves not conducted, more Ps than QRSs
action of antiarrhythmic agents correct arrhythmias by a variety of mechanisms, depending on the group used
lab test considerations of antiarrhythmic agents renal & hepatic functions & serum potassium levels should be evaluated periodically throughout therapy, may cause elevated serum BUN cholesterol & triglyceride levels, may cause decreased blood glucose concentrations
pacemaker battery-operated device that initiates & controls the heart rate used for dradydysrhythmias, tachydysrhythmias, or 2nd & 3rd heart block either temporary or permanently
inpatient cardiac rehab most commonly initiated _____________ time of a cardiac event
nursing care in inpatient cardiac rehab VS, O2, exercise, contraindications, patient teaching
contraindications for inpatient cardiac rehab unstable angina, ischemic changes to resting ECG, resting systolic BP >200 or diastolic >110, acute systemic illness or fever, uncontrolled arrhythmias, uncontrolled sinus tachy, uncompensated CHF, 3rd degree AV block, pericarditis, myocarditis, DM
goals of outpatient cardiac rehab strength & flexibility are the same as inpatient cardiac rehab
recovery-you know that you've done too much (outpatient cardiac rehab) become exhausted, cold sweat, light-headed, feel nauseated, SOB, chest pain or discomfort
cardiac rehab patient may resume sexual activity when? many about a month after a heart attack check with physician
best exercise for cardiac rehab walking
risk factors that affect cardiac rehab DM, high BP, cholesterol, overweight, physical inactivity, smoking, stress management, cardiac medications
Created by: ealongo