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Cardiovascular
phase 2 test 7 (revised)
| Question | Answer |
|---|---|
| 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
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