Lecture 5: Cardiovascular System Flashcards
1
Q
Contents of Heart
A
- look at picture on page 1
- epicardium is part of parietal pericardium
2
Q
CVD
A
- leading cause of death in US
- MI primary cause
3
Q
Oxygen Balancing Act
A
- critical balance between myocardial oxygen supply and demand
- 4 major determinants of myocardial oxygen demand: HR, contractile force, muscle mass, ventricular wall tension
- hearts law of supply and demand: if myocardial oxygen demand increases, so must oxygen supply
- tissue hypoxia (partial blockage of blood flow to the heart or body): causes coronary arteries to dilate and increases coronary blood flow
- stenotic, diseased valves cannot dilate: may result in oxygen deficit
- cardiac workload and oxygen demand increases if HR speeds up force of contraction becomes stronger
- one way flow: valves open and close in response to pressure gradient
- decreased flow: valvular disease-allows blood to flow backward across leaflets (regurgitation), valve may become restricted (stenosis), forces to pump more blood increasing cardiac workload–>can result in backflow or spillage into other areas (problem)
- if arterial pressure falls below normal (hypotension), then increase occurs in HR, force of contraction, constriction of arterioles (want to bring pressure back up)
- if arterial pressure rises above normal (hypertension), then you have reflex slowing of heart, decrease of contraction, vasodilation
4
Q
CV Risk Factors: Modifiable that Reduce Incidence of CVD
A
- cigarette smoking is leading preventable cause: increases HR and BP and narrows blood vessels
- quit decrease risk of CAD by 1/2 after one year and is same as nonsmoker after 15 years-nicotine enhances likelihood of stenosis because of plaque build up
- elevated total serum cholesterol levels >200
- HTN: aggravated by obesity and as related to diabetes mellitus and regular alcohol use
5
Q
CV Risk Factors: Modifiable that are Likely to Reduce CVD
A
- obesity
- physical activity
- impaired glucose metabolism (associated with DM)
- low HDL levels
- hormonal status
6
Q
CV Risk Factors: Might Reduce CVD
A
- psychological factors and emotional stress (3x more likely to have 2nd MI if anxious, negative, type D personality)
- moderate alcohol consumption or taking in dietary supplements with flavonoids and antioxidants
7
Q
CV Risk Factors: Non Modifiable
A
- age
- gender
- family history
- ethnicity
8
Q
S&S of CVD
A
- chest pain and discomfort (may radiate into neck, jaw, upper traps, upper back, shoulder or arms
- angina
- palpitations
- dyspnea
- cardiac syncope: lightheadedness, fainting; caused by reduced oxygen to brain d/t cardiac related disorder
- fatigue: provoked by maximal exertion
- cough
- cyanosis
- peripheral edema
- claudication
9
Q
S&S CVD: Angina
A
- chest pain or discomfort when a heart muscle does not get enough oxygen (pressure, squeezing or tightness)
- often mistaken for indigestion
- a symptom of coronary artery disease
10
Q
S&S CVD: Palpitations
A
- aka arrhythmias or dysrhythmias (presence of irregular heartbeat)
- described as pound, jump, flop, flutter, or racing sensation of heart
- benign (>6/minute) or severe
11
Q
S&S CVD: Dyspnea
A
- means breathlessness or SOB
- DOE: dyspnea on exertion (mild exertion)
- PND: paroxysmal nocturnal dyspnea-sudden, unexplained episodes of SOB that awaken a person sleeping in supine position; caused by peripheral fluid being returned to heart and lungs which become overwhelmed-often comes with CHF
- orthopnea: breathlessness relieved by sitting upright
- cardiac cause is often impaired left ventricle
12
Q
S&S CVD: Cyanosis
A
- bluish discoloration of lips, nail beds, fingers and/or toes
- due to problem in blood oxygen levels
13
Q
S&S CVD: Peripheral Edema
A
- hallmark of right ventricle failure
- usually bilateral and dependent
14
Q
S&S CVD: Claudication
A
- cramping or pain in legs with activity
- caused by CVD
- usually brought on by consistent amount of exercise and activity
15
Q
Aging and CV System: Specific Effects
A
- hearts of older people pump less blood and work much harder under same circumstances than do their younger counterparts
- arterial walls become stiffer due to many factors
16
Q
Aging and CV System: Effects on Function
A
- these changes have consequences during CV stress, but not necessarily at rest
- age is greatest risk factor for CVD-decreases functional capacity
17
Q
Aging and CV System: Exercise
A
- can partially reverse some of age-associated changes
- age related changes may be due to inactivity (main culprit)
18
Q
CAD in Women
A
- single leading cause of death
- less likely to get preventative care, invasive treatments, thrombolytic therapy within 60 minutes
- decision delay
- first heart attack more severe
- do just as well after surgical revascularization
- 2x as likely to die within 1 year after heart attack
- greater risk for second heart attack and for disability because of heart failure
- hormonal status: estrogen-cardioprotective effect on CV system, CAD rates match men within 10 years of menopause; hormone replacement for postmenopausal women-doesn’t help CAD or protect against MI; oral contraceptives-if over 35 and use them and smoke, increased risk of heart attack and stroke
19
Q
HTN in Women
A
- more women than men develop
- white coat HTN more common (anxiety provoked because in medical environment results in increased BP reading)
- HTN among black people more common in women
- LVH more often fatal in women
20
Q
Acute Coronary Syndromes
A
- MI
- angina pectoris
21
Q
MI: Definition and Incidence and Risk Factors
A
- reduced blood flow through one of the coronary arteries
- development of ischemia with resultant necrosis of myocardial tissue
- leading cause of death in adult american population
- RF…
- diabetes
- family history of heart disease
- hyperlipoproteinemia
- HTN
- menopause
- smoking
- stress
- high fat/CHO/salt diet
22
Q
MI: Pathogenesis, Clinical Manifestations, and Medical Management
A
- pathogenesis: tissue death followed by inflammatory process then remodeling to form a scar in 6-8 weeks
- CM: chest pain usually in substernal chest (unrelieved by rest or nitroglycerin), anxiety, fatigue, pallor, SOB, diaphoresis (excessive sweating), nausea and vomiting
- prevention: same for all CVD
- dx: clinical history, ECG, cardiac enzymes
- tx: reestablish flow of blood in blocked coronary arteries
- prognosis: depends on size of MI, age, other CVD, respiratory disease, uncontrolled DM, hypotension
23
Q
Angina Pectoris: Definition, Overview, Etiology, and Risk Factors
A
- when cardiac workload exceeds oxygen supply to myocardial tissue, ischemia occurs
- chronic stable angina: aka exertional angina-predictable, occurs with physical exertion/emotional stress, no pain at rest
- unstable angina: unpredictable, lasts > 15 minutes, symptom of worsening cardiac ischemia
- variant angina: d/t coronary artery spasm, usually in early morning, unrelated to exertion
- any condition that alters blood/oxygen supply or demand of the myocardium leading to ischemia, usually CAD
24
Q
Angina Pectoris: Pathogenesis, Clinical Manifestations, Medical Management
A
- symptom of ischemia due to imbalance of oxygen supply and cardiac workload; blockage or partial blockage with disruption of a formed plaque
- clinical manifestations: pain, squeezing, burning, pressing, heartburn, indigestion or choking; chest, left shoulder and down ulnar border L arm, back of neck, lower jaw, teeth, left upper back, interscapular, abdomen, right arm; usually lasts 1-3 minutes, but may persist for up to 20; may manifest differently in women
- dx: history, relief by nitroglycerin
- prevention and tx: treat underlying disorders, nitroglycerin, beta-blockers, calcium-channel blockers, aspirin, revascularization
- prognosis: 1/3 die from MI
25
Q
Aortic Aneurysm: Overview, Incidence, Etiologic Factors and Pathogenesis
A
- abnormal dilation 50% greater than normal
- usually occurs between renal arteries and iliac branches
- incidence increases with age
- more common in men
- 50% have HTN (seems in increase aneurysm formation, systemic pressure pounds against walls of arteries–>stretches them out)
- caused by injury or atherosclerosis to tunica media (about 95% of AAA result from arteriosclerosis)
- measures 6 cm has 20% rupture within a year
26
Q
Aortic Aneurysm: Clinical Manifestations, Medical Management
A
- may be asymptomatic but depends on size, position, and rate of growth
- early warning signs may include abdominal heartbeat when lying down
- S&S of enlargement and rupture: weakness, sweating, tachycardia, hypotension
- dx: palpation, radiography, ultrasound, echocardiography, arteriography, aortography
- prevention and treatment: family hx, smoking cessation, regular exercise, BP control, cholesterol management, surgery, if small beta-blockers (decrease BP)
- prognosis: with open surgery there is high morbidity and substantial mortality rate; aneurysm rupture is associated with a high mortality rate
- dissecting aneurysm: bleeding into a weakened artery causes artery wall to split
27
Q
Cardiac Tamponade: Overview, Pathogenesis
A
- pressure on heart that adversely affects function
- rapid rise in intrapericardial pressure from blood or fluid accumulation in pericardial sac: impairs diastolic filling of heart, reduces amount of blood that can be pumped out with each contraction; if left untreated cardiogenic shock and death can occur
28
Q
Cardiac Tomponade: Clinical Manifestations and Medical Management
A
- beck’s triad
- orthopnea
- diaphoresis
- anxiety
- restlessness
- pulsus paradoxus: abnormally large decrease in systolic BP during inspiration
- cyanosis
- weak rapid peripheral pulse
- dx: chest x-ray, ECG, echocardiography, pulmonary artery pressure monitoring
- tx: pericardiocentesis, surgery, insertion of drain into pericardial sac
29
Q
Beck’s Triad for Cardiac Tamponade
A
- hypotension with narrowing pulse pressure
- elevated central venous pressure with neck vein distention
- muffled heart sounds
30
Q
Cardiogenic Shock: Overview, Etiology, Pathogenesis
A
- called pump failure
- diminished CO that impairs tissue perfusion and oxygen delivery
- reflects severe left-sided heart failure
- infarction typically exceeds 40% of hearts muscle mass
- most common cause is acute MI
- pathogenesis: left ventricular dysfunction triggers series of compensatory mechanisms to increase CO: initially stabilizes patient, but later causes deterioration d/t increase oxygen demands resulting in a vicious cycle of decompensation
- as CO falls baroreceptors in aorta and carotid arteries initiate responses in SNS which increases HR, LV filling pressure, and peripheral resistance to enhance venous return
31
Q
Cardiogenic Shock: Clinical Manifestations, Medical Management
A
- cold, pale, clammy skin
- drop in systolic pressure to 30 mm Hg below baseline
- weak peripheral pulses
- tachycardia
- rapid, shallow respirations
- restlessness
- confusion
- cyanosis
- dx: pulmonary artery pressure monitoring, invasive arterial pressure monitoring, arterial blood gases, ECG, cardiac enzymes, echocardiography
- tx: cardiovascular drugs, intra-aortic balloon pump
- prognosis: poor unless you get it under control
32
Q
Types of Cardiomyopathy
A
- dialated
- hypertrophic
33
Q
Dilated Cardiomyopathy
A
- disease of heart muscle fibers, usually not diagnosed until advanced stages
- pathogenesis: involves hypodynamic ventricular myocardium, grossly dilates every heart chamber as a result of increased volumes and pressures
- CM: SOB, orthopnea, DOE, fatigue, dry cough, peripheral edema, irregular pulse, nausea
- dx: ECG and angiography, chest x-ray, echocardiography, cardiac catheterization
- tx: correct underlying cause, improve hearts pumping ability (drugs)
- prognosis: most die within 2 years of symptom onset
- CO remains low and have to go into compensatory mode to counteract usually ends badly
34
Q
Hypertrophic Cardiomyopathy
A
- primary disease of cardiac muscle
- course of disorder varies
- 50% of all cases genetically transmitted
- pathogenesis: LVH-causes increased resistance to blood entering right ventricle and an increase in diastolic filling pressures, eventually causes pump failure
- CM: systolic ejection murmur, SOB, orthopnea, DOE, fatigue, angina, syncope, activity intolerance, atrial fibrillation, chest pain
- dx: ECG, chest x-ray, echocardiography, cardiac catheterization
- tx: relax ventricle-relieve outflow tract destruction, drugs
35
Q
CAD: Overview, Pathogenesis
A
- leading cause of death
- blockage of blood flow to coronary arteries
- pathogenesis: results with atherosclerotic plaque fills lumens of coronary arteries; obstructs blood flow to heart leading to ischemia and eventually necrosis
- arteriosclerosis: thickening and loss of elasticity of arterial walls
- atherosclerosis: plaques of fatty deposits form in intima…most common
- combo of hypoxia, decreased energy availability, and acidosis impairs LV function: less blood ejected from heart
36
Q
CAD: Clinical Manifestations and Medical Management
A
- angina pectoris
- MI
- sudden death
- prevention: change modifiable risk factors, slow growth of plaque
- dx: ECG, coronary angiography; exercise treadmill testing; thermography
- exercise and physical activity: exercise is one single intervention with ability to influence greatest number of risk factors
- tx: reduce myocardial oxygen demand or increase oxygen supply; drugs; invasive measures-PTCA, CABG, laser angioplasty
- prognosis: comprehensive risk factor reduction will extend survival, improve quality of life, decrease need for procedures, and reduce incidence of subsequent MI
- postoperative exercise-CR
37
Q
Ineffective Endocarditis
A
- strep or staph infection of lining inside heart including valves
- most commonly affecting mitral
- risk factors: dental procedures, immunodeficiency, IV drug use, surgery, artificial heart valves
- pathogenesis: inflammation of cardiac endothelium, destruction of connective tissue d/t bacterial lytic enzymes, vegetations form (fibrin and platelet thrombi) can break off and cause sepsis
- CM: similar to bacterial infections; malaise, weakness, fatigue, weight loss, anorexia, arthralgia, night sweats, chills, valvular insufficiency, intermittent fever
- dx: blood cultures
- tx: antibiotics
- prognosis: difficult to treat and can result in serious heart damage or death: insidious onset, don’t really know what it is when it starts
38
Q
Heart Failure: Overview, Types, Etiology
A
- heart unable to pump sufficient blood to supply the body’s needs–backup of blood into pulmonary veins and get increased pressure in pulmonary capillaries
- usually occurs in damaged LV but can occur in right
- results in intravascular and interstitial volume overload and poor tissue perfusion (not getting to tissues)
- 4 types: systolic heart failure, diastolic failure, left-sided heart failure (CHF) and right-sided heart failure (cor pulmonale)
- common complication of ischemic and HTN heart disease
- those with pre-existing heart disease
- etiology: impaired ventricular function and arrhythmias; mechanical disturbances: mitral stenosis or atrial fibrillation; systolic hemodynamic disturbances: mitral or aortic insufficiency (leads to volume overload), aortic stenosis or systemic HTN (cause increased resistance to ventricular emptying and decreased CO)
39
Q
Heart Failure: Pathogenesis, Clinical Manifestations, Medical Management
A
- increased workload and end-diastolic volume enlarge LV: body responds to compensate
- CM: left-sided heart failure: progressive dyspnea, orthopnea, pulmonary edema, fatigue, muscular weakness, renal changes; right sided heart failure: dependent edema, JVD, abdominal pain, RUQ pain d/t liver congestion, anorexia, nausea, cyanosis
- dx: clinical picture to distinguish L from R failure; echocardiogram is main tool
- prevention and treatment: improve pump function to reverse compensatory mechanisms, drugs, low salt diet and restricted fluid intake, medications, and exercise
40
Q
Left-Sided CHF
A
- LV weakens and cannot empty
- decreased CO to system
- decreased renal blood flow stimulates renin-angiotensin and aldosterone secretion
- backup of blood into pulmonary vein
- high pressure in pulmonary capillaries leads to pulmonary congestion or edema
41
Q
Right-Sided CHF
A
- RV weakens and cannot empty
- decreased CO to system
- decreased renal blood flow stimulates renin-angiotensin and aldosterone secretion
- backup of blood into systemic circulation (venae cavae)
- increased venous pressure results in edema in legs and liver and abdominal organs
- very high venous pressure causes distended neck vein and cerebral edema
42
Q
Hypertension: Overview, Incidence, Etiology and Risk Factors
A
- systolic >/140 vs diastolic >/ 90
- 50 M adult Americans
- 2x more prevalent and severe among black people
- etiology and risk factors: primary (essential)-genetics, smoking, obesity, HC, increased sodium intake, sedentary lifestyle, race (black people more prevalent); secondary-related to systemic disease that increases peripheral vascular resistance or CO–renovascular disease, cushing’s syndrome, primary aldosteronism, DM, pregnancy, CRF, RAS, endocrine disease
43
Q
Hypertension: How It Happens
A
- changes in arteriolar bed causes increased TPR
- abnormally increased tone in SNS causes increased TPR
- abnormal renin release results in formation of angiotensin II which constricts arterioles and increases blood volume
44
Q
Hypertension: Pathogenesis, Clinical Manifestations, Medical Management
A
- patho: blood flow-determined by CO or TPR or both; PVR-determined by diameter of vessels; increases heart’s workload-causes LVH and leads to left-sided heart failure, pulmonary edema and right-sided heart failure
- CM: frequently asymptomatic-doesn’t produce signs until vascular changes in heart, brain, or kidney occur: dizziness, confusion, fatigue, blurred vision, nocturia, edema
- prevention: know BP, physical activity, weight control, limitations on salt and alcohol intake
- dx: BP over 140/90, urinalysis and excretory urography, serum potassium levels, BUN and creatinine levels (high levels suggest renal disease), ECG to detect LVH or ischemia, chest x-ray (enlarged heart as a result of HTN)
- tx: take into account all risk factors not just BP numbers
- prognosis: good if treated; if untreated, 50% will die of heart disease, 33% of stroke, 15% of renal failure
45
Q
Hypovolemic Shock
A
- reduced intravascular volume causes circulatory dysfunction and inadequate tissue perfusion
- caused by acute blood loss
- body’s compensatory mechanisms can’t maintain circulation
- pathogenesis: BP decreases –> compensatory mechanisms increase cardiac output –> compensatory mechanisms increase sodium and water retention –> compensatory mechanisms (release ADH) stimulates thirst –> compensatory mechanisms fail –> BP decreases and tissue perfusion is impaired –> oxygen and nutrient delivery to cells decreases –> cardiac ischemia and arrhythmias may develop
- CM: cyanosis, metabolic acidosis, cool clammy skin, weak thready pulse
- medical management; adequate airway, ensuring ventilation, and maximizing circulation; direct pressure should be applied to external bleeding vessels to prevent further blood loss; starting IV lines or splinting of extremities
46
Q
Myocarditis
A
- acute or chronic focal or diffuse inflammation of cardiac muscle
- patho: infectious organism triggers autoimmune, cellular and humoral reaction, resulting inflammation may lead to hypertrophy, fibrosis, and inflammatory changes, heart muscle weakens and contractility decreases, heart muscle becomes flabby and dilated
- CM: fatigue, dyspnea, palpitations, fever, continuous chest pressure or soreness, tachycardia, peripheral edema
- MM: detection of dysrhythmia with cardiac monitoring, administration of supplemental oxygen, and management of fluid status
47
Q
Pericarditis
A
- inflammation of pericardium; acute: fibrinous or effusive, chronic: constrictive-dense fibrous pericardial thickening
- etiology: bacterial, fungal, or viral infection, neoplasms, high-dose radiation to chest, hypersensitivity or autoimmune disease, drugs
- patho: may lead to cardiac tamponade (pressure on heart) or pericardial effusion (fluid accumulates within pericardial sac)
- CM: chest pain made worse by lying down and by respiratory movements (shallow, rapid respirations), friction rub-high pitched scratch sound heard at end-expiration when auscultating
- dx: ESr elevated, pericardial fluid culture, BUN levels, ECG, echocardiography, auscultation
- tx: antibiotics, symptomatic treatment (bed rest), pericardiocentesis
- prognosis: depends, typically good in acute cases
48
Q
Rheumatic Fever/Heart Disease: Overview and Etiology
A
- systemic inflammatory disease of childhood
- after infection of upper respiratory tract
- involves heart, joints, CNS, skin, and subcutaneous tissue: if not treated, scarring deformities of cardiac structures result in rheumatic heart disease
- disease strikes during cool, damp weather
- etiologic factors: genetic predisposition, hypersensitivity reaction-may have altered immune response in development and recurrence; mitral and aortic valves are completely destroyed-severe heart inflammation (develops in 50% of patients with rheumatic fever, which can result in heart valve damage)
49
Q
Rheumatic Fever/Heart Disease: Clinical Manifestations and Medical Management
A
- endocarditis: causes leaflet valve swelling and fibrin deposits, affects mitral valve most commonly in females and aortic in males, affects tricuspid valves in both
- joint pain
- swelling, redness, and signs of effusion
- 5% develop a rash
- dx: WBC count and ESR, positive c-reactive protein, increased cardiac enzymes, echocardiography, cardiac catheterization
- tx: eradicate streptococcal infection, may need corrective surgery (valve replacement)
- prognosis: of those who survive 20% die within 10 years
50
Q
Valvular Heart Disease
A
- mitral stenosis
- mitral regurgitation (insufficiency)
- mitral valve prolapse
- aortic stenosis
- aortic regurgitation
51
Q
Mitral Stenosis
A
- narrowing of MV by abnormalities, calcification, or fibrosis: obstructs blood flow from LA to LV; LA volume and pressure rise-gives increased resistance to blood flow causing pulmonary HTN, RVH, and right sided heart failure, decreased CO d/t inadequate filling of LV
- etiology and patho: sequela of rheumatic fever, mitral valve is thickened, endocarditis
- CM: angina, orthopnea, dyspnea and fatigue, pulmonary venous congestion, a-fib, RV failure, pulmonary edema
- dx: echocardiography
- tx: valve repair or replacement
- prognosis: good
52
Q
Mitral Regurgitation
A
- abnormality of mitral leaflets, chordae tendinae, papillary muscles, left atrium or LV
- etiology and patho: blood from LV flows back into LA during systole –> atrium enlarges, LV dilates to accommodate increased blood volume from atrium (also compensates for decreased CO), ventricular hypertrophy and increased end-diastolic pressure result in increased pulmonary artery pressure –> L and R sided heart failure
- mitral valve prolapse
- dilated cardiomyopathy
- rheumatic fever
- MI
- rupture of chordae tendinae
- CM: PND, DOE, exercise-induced fatigue, weakness, a-fib
- dx, tx, and prognosis: auscultation or echocardiography, surgery for repair or replacement
53
Q
Mitral Valve Prolapse
A
- billowing and improper closing of mitral valve
- part of valve billows back into LA during LV contraction –> mitral valve regurgitation
- etiology and patho: anatomic abnormality-variation in shape of mitral valve
- CM: dizziness, syncope, palpitations, profound fatigue, chest pain, heart murmur
- dx: auscultation and echocardiography
- tx: beta blockers, exercise program, elimination of caffeine, alcohol, and tobacco
- prognosis: benign condition in vast majority not life threatening
54
Q
Aortic Stenosis
A
- narrowing of aortic valve
- etiology and patho: increased LV pressure tries to overcome resistance of narrowed valvular opening: increases demand for oxygen, decreases CO causes poor coronary artery perfusion, ischemia of LV and L sided heart failure; progressive valvular calcification, congenital aortic bicuspid valve, rheumatic fever, atherosclerosis
- halmar findings of ventricular failure: decreased ejection fraction
- CM: dyspnea, angina, exertional syncope
- dx: echo-doppler, ECG, x-ray
- tx: surgery for replacement, balloon valvuloplasty
- prognosis: good if asymptomatic or valve replaced; poor if symptomatic
55
Q
Aortic Regurgitation
A
- incomplete closure aortic valve
- etiology and patho: scarring and retraction of valve leaflets; blood flows back into LV during diastole-causes fluid overload in ventricle, which dilates and hypertrophies, leads to fluid overload in LA and then in pulmonary system, left-sided heart failure results; acute: infective endocarditis, chest trauma, prosthetic valve dysfunction, acute ascending aortic dissection; chronic: HTN, rheumatic fever, Marfan syndrome, ankylosing spondylitis, syphilis, ventricular septal defect
- CM: DOE, fatigue, exercise intolerance, PND, pulmonary edema, angina
dx: echocardiography with doppler - tx: surgical reconstruction or replacement (recommended before permanent damage happens)
- prognosis: poor with chronic regurgitation
56
Q
Peripheral Vascular Disease
A
- arterial occlusive diseases: arteriosclerosis obliterans (PAD)
- venous diseases: venous thrombosis and pulmonary embolus, and varicose veins
57
Q
Arteriosclerosis Obliterans
A
- proliferation of intima has caused complete obliteration of the lumen of artery, most common arterial occlusive disease
- etiology, pathogenesis and RF same as CAD
- CM: claudication, pain, pallor, paresthesia, paralysis, pulselessness, lower SBP at ankle than at arm
- dx: client hx and clinical exam, ABI and arteriography
- prevention: smoking cessation, dietary management, exercise (increases collateralization of blood vessels)
- tx: aspirin, surgery
- prognosis: depends
58
Q
Venous Thrombosis and Pulmonary Embolus: Overview and Etiologic and Risk Factors
A
- partial or complete occlusion of vein by thrombus (intravascular collection of platelets, erythrocytes, leukocytes, and fibrin)
- two types of venous thrombosis: superficial (usually saphenous vein)-usually result of varicose veins, self-limiting not serious; or deep (DVT-usually femoral or iliac veins)-distal are usually clinically silent and benign, proximal more likely to become PE’s
- PE: embolism lodged in pulmonary circulation; S&S-sudden death, pain, tachypnea, tachycardia, anxiety
- etiologic and risk factors: high risk post-surgery, venous stasis, hypercoagulability, or injury to venous wall
59
Q
Venous Thrombosis and Pulmonary Embolus: Pathogenesis, Clinical Manifestations, and Medical Management
A
- trauma to endothelium initiating thrombosis
- CM: dull ache, tight feeling, pain, swelling, tenderness, warmth
- dx: wells clinical decision rule, do not use homan’s test
- prevention: early mobilization for low risk, anticoagulants for moderate to high risk, knee elastic stockings (keep pressure and enhance blood flow), pneumatic pressure devices, ankle pumping
- tx: low molecular weight heparin and then warfarin
- prognosis; without complications 1 to 3 weeks to normal for distal (calf) DVT and within 6 weeks for proximal (thigh or pelvic)
60
Q
Varicose Veins
A
- abnormal dilation of veins leading to tortuosity, valve incompetence, and propensity to thrombosis
- etiologic and risk factors: may be inherited; periods of high venous pressure
- patho: pooling of blood secondary to valve incompetence
- CM: visible dilated veins, dull aching heaviness, tension, feeling of fatigue, cramps
- dx: look at it
- tx: leg elevation, elastic stockings, surgery
- prognosis: good
