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DPT 724 Pathophysiology > Lecture 5: Cardiovascular System > Flashcards

Lecture 5: Cardiovascular System Flashcards

1
Q

Contents of Heart

A
  • look at picture on page 1

- epicardium is part of parietal pericardium

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2
Q

CVD

A
  • leading cause of death in US

- MI primary cause

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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
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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
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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
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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
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7
Q

CV Risk Factors: Non Modifiable

A
  • age
  • gender
  • family history
  • ethnicity
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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
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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
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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
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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
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12
Q

S&S CVD: Cyanosis

A
  • bluish discoloration of lips, nail beds, fingers and/or toes
  • due to problem in blood oxygen levels
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13
Q

S&S CVD: Peripheral Edema

A
  • hallmark of right ventricle failure

- usually bilateral and dependent

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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
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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
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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
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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)

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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
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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
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20
Q

Acute Coronary Syndromes

A
  • MI

- angina pectoris

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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
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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
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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
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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
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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
  1. LV weakens and cannot empty
  2. decreased CO to system
  3. decreased renal blood flow stimulates renin-angiotensin and aldosterone secretion
  4. backup of blood into pulmonary vein
  5. high pressure in pulmonary capillaries leads to pulmonary congestion or edema
41
Q

Right-Sided CHF

A
  1. RV weakens and cannot empty
  2. decreased CO to system
  3. decreased renal blood flow stimulates renin-angiotensin and aldosterone secretion
  4. backup of blood into systemic circulation (venae cavae)
  5. increased venous pressure results in edema in legs and liver and abdominal organs
  6. 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

DPT 724 Pathophysiology (18 decks)

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