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49 Cards in this Set
- Front
- Back
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Major Cardiovascular Diseases according to the AHA |
- ischemic (coronary) heart disease - hypertension - heart failure - cerebrovascular disease (stroke) |
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Atherosclerosis |
- atherosclerotic plaques are composed of lipid and thrombus |
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Atherosis |
- fatty streak that consists of lipid-laden macrophages and smooth muscle cells |
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Sclerosis |
- Responsiblefor reduction of blood vessel compliance - Organization of “fibrous cap”of thrombi over advanced plaques that have developed on endothelial lining
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Vasospasm |
- hyperplasia of intimal smooth muscle cells is hallmark of advanced atherosclerosis creatinga coronary artery that is prone to spasm |
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Prinzmetal angina |
- variant angina associated with ST-segment elevation, at rest, and not associated with any preceding increase in myocardial oxygen demand |
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Risk Factors and Cardiovascular Disease |
- Framingham Study tested relationship between genetic and behavioral factors and contribution to development of coronary atherosclerosis - The greater the number of risk factors present, the greater the likelihood that CAD, and ultimately CHD, will exist |
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Cardiovascular Disease: Risk Factors |
- smoking - physical inactivity, obesity - diabetes, suboptimal diet - hypertension - elevated serum total cholesterol >> elevated LDL >> decreased HDL - family history - age, gender - stress |
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CV Disease: Modifiable Risk Factors |
- Cigarette/ tobacco smoking - High blood pressure (over 140/90) - High blood cholesterol levels—best predictoris ratio of totalcholesterol to HDL - Physicalinactivity |
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CV Disease: Non-Modifiable Risk Factors |
- Heredity - Male sex - Increased age |
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Risk Factors: Diabetes |
nonenzymaticglycosylation, or the chemical attachment of glucose to proteins without enzymes affects fibrinogen, collagen, and antithrombin III, HDL, and LDL |
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Risk Factors: Obesity |
BMI≥ 30kg/m2 |
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Risk Factors: Family Hx |
parent or sibling
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Risk Factors: Gender and Age |
- increased age - before 55yrs, men 6x more likely than women to have MI - CHD is the second leading cause of death in all women <45 years |
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Risk Factors: Stress |
- sense of time urgency and easily aroused hostility or type A behavior |
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Emerging Risk Factors |
- Lipoproteina - LDL subclasses - Oxidized LDL - Homocysteine - Hematological factors - Inflammatory markers - Infective agents such as Chlamydia Pneumoniae |
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Clinical Course: 1 of 4 ways |
- Sudden cardiac death - Chronic stable angina - Acute coronary syndrome(ACS) >> Unstable angina >> ST-segment elevation myocardial infarction (STEMI) >> Non-STEMI - Cardiac muscle dysfunction |
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Cardiac vs. Musculoskeletal |
- cardiac chest pain is related to effort, tired, sweating, etc. - Chest Wall: rib cage, bone problem, tenderness with palpation; not much pain change with exercise but hurts if chest wall moves - don't have other sx like fatigue, malaise, - if working and PT feels pain – stop and if sx reduce, then may be cardiac. Check HR & BP, if return to normal at rest then is ok |
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Chronic Stable Angina |
- Well-established level of onset - Result of not enough blood supply to meet metabolic demand - Usually can control symptoms by reducing the intensity of exercise or taking sublingual nitroglycerin |
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Acute Coronary Syndrome |
- Unstable angina: chest discomfort that is accelerating in frequency or severity, may occur at rest - Acute myocardial infarction |
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Factors that contribute to unstable angina |
- Circadian variations in catecholamine levels - Increases in plasma viscosity - Increases in platelet activation - Pathological changes in atherosclerotic plaques |
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STEMI |
- develops a Q wave on ECG in subsequent 24 to 48 hours (transmural infarction) |
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Non-STEMI |
doesnot develop a Q wave on ECG (referred to nontransmural or subendocardial region infarction) |
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Medical management of acute coronary syndrome |
- Primary concern for management is to reperfuse the area of heart not receiving enough blood and oxygen - Control for cardiac pain—nitrates, morphine, beta-blockers - Limit any amount of necrosis - Prevent complications - Fibrinolysis and PTCA if within 3 hours of onset - Aspirin Improve oxygenation - Limitation of infarct size - Prophylaxis for arrhythmias - Control of other complications |
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Complications with STEMI and non-STEMI |
- abnormal contraction patterns >> Dyssynchrony >> Hypokinesis >> Akinesis >> Dyskinesis - Persistent angina and arrhythmias (STEMI) |
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Ventricular Remodeling |
- With STEMI, changes in shape, size, and thickness of myocardium - Areasof ventricular dilation and ventricular hypertrophy - Factors that affect remodeling >> Size of infarct >> Ventricular load >> Patency of the artery that was infarcted |
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Prognosis |
Related to complications, infarction size, presence of disease on other coronary arteries, and left ventricular function *Natural history of coronary disease - Little is known about natural history - Knowledge of risk factors can assist in determining relative risk - Secondary prevention methods |
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Hypertension Values |
- normal <120 S/ <80 D - high normal 120-139/ 80-89 - hypertension stage 1: 140-159/ 90-99 - hypertension stage 2: >159/ >99 |
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Hypertensive Heart Disease |
- Producesa pressure overload on left ventricle - Diastolic dysfunction with impairment of LV relaxation develops early |
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Systemic Effects of Uncontrolled Hypertension |
- Brain - Atherosclerosis - Heart - Kidney - Eyes - Blood Pressure |
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Systemic Effects of Uncontrolled Hypertension: Brain |
cerebral aneurysm, hemorrhagic CVA (stroke) |
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Systemic Effects of Uncontrolled Hypertension: Heart |
- congestive heart failure - atherosclerosis - angina - myocardial infarction |
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Systemic Effects of Uncontrolled Hypertension: Kidney |
- nephrosclerosis - chronic renal failure |
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Systemic Effects of Uncontrolled Hypertension: Eyes |
- retinopathy: arteriolar damage, with micro aneurysms and rupture |
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Systemic Effects of Uncontrolled Hypertension: Blood Pressure |
persistent evaluation |
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Systolic Dysfunction |
an impairment in ventricular contraction, resulting in decrease in stroke volume and decrease in ejection fraction (<40%). An increase in end systolic volume will also occur. Now called heart failure with reduced ejection fraction or HFREF. |
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Diastolic Dysfunction |
changes in ventricular diastolic properties that lead to an impairment in ventricular filing (reduction in ventricular compliance) and an impairment in ventricular relaxation. A consequence of diastolic dysfunction is the rise in end diastolic pressure. Now called heart failure with preserved ejection fraction or HFPEF. |
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Treatment Goals for Hypertension |
- normalize BP both at rest and during exertion; reverse LVH and myocardial dysfunction |
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Treatment for Hypertension: Prehypertension |
lifestyle modification |
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Treatment for Hypertension: Stage 1 |
- thiazide diuretics
- may consider angiotensin-converting enzyme (ACE) inhibitor, angiotensin II receptor blockers, beta blocker, calcium-channel blocker |
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Treatment for Hypertension: Stage 2 |
- two-drug combination - thiazide and ACE or other |
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Hypertension and Exercise |
- Exercise capacity is reduced by 15% to 30% - Stroke volume increases subnormally and peak heart rate is lower reducing cardiac output - Exercise leads to reductions in both systolic and diastolic BP |
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Implications for physical therapy intervention |
- high percentage of patients referred to physical therapy will have recognized or unrecognized HTN - Should include monitoring during treatment sessions - Refer to physician if resting BPis high (SBP >200mm Hg or DBP >100 mm Hg) |
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Peripheral ArterialDisease (PAD) |
- PAD is referred to as atherosclerotic occlusive disease (AOD) - Atheromatous plaque obstruction of large or medium-sized arteries supplying blood tothe extremities |
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PAD and Exercise |
- Patients are unable to produce normal increases in peripheral blood flow - Intermittent claudication leads to moderate to severe impairment in walking ability - Exercise has improved pain-free and maximal walking tolerance on level ground and during constant-load treadmill exercise |
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PAD and Implications for physical therapy intervention |
- All patients should receive heart rate and BP monitoring during PT evaluation |
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S&S Arterial Insufficiency |
- painful walking (intermittent claudication) - elevated foot develops increased pallor - venous filling delayed following foot elevation - redness of distal limb (dependent rubor) - death of tissue (gangrene) |
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DVT Assessment |
- Wells Score - DVT 'likely' 2 points or more - DVT 'unlikely' fewer than 2 points |
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Aortic Aneurysm: Implications for PT |
- check for pulsating tumor/mass in abdominal area - Bruitheardover swollen area in abdomen - Pressure on surrounding parts such as low back - Leg pain/ claudication pain - Numbness in lower extremities - excessive fatigue - Poor distal pulses - Low back pain |
