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APK4120 Final
| Question | Answer |
|---|---|
| What is main focus of clinical ex physio | the interplay of exercise and chronic disease |
| Three main questions of clinical ex physio | how does exercise influence the disease process, how does ex testing indicate the presence of disease and help diagnose, how role does ex play in treatment or pevention |
| 4 main duties of a CEP | analyze history to assess risk and prescribe rx, perform gxts and stress tests, measure BP/02/heart rhythm/health indicators, develop ex rx to im prove health |
| 4 aspects of CEP knowledge | anatomy, physiology, chemistry, psychology |
| CEP degree & knowledge requirements | minimum bachelors, possibly masters, and a clinical internship |
| Most common work setting for CEPs | cardiac rehab |
| Main work settings for CEPs | hospitals, outpatient clinics, physician offices, research facilities |
| Designated CEP professional organization | CEPA, clinical exercise physiology association |
| Scope of practice for a CEP | it varies by organization, CEPA vs ACSM vs ACE vs CSEP |
| What does the CEPA define the scope of a CEP as | master’s degree related to ex. science and/or licensed OR holds a clinical ex certification i.e. ACSM CEP |
| What is the one state that requires a state license of a CEP | louisiana |
| Why is licensure important | ensures the same knowledge and scope across practices to prevent variation |
| Main goals of licensure movements | recognition of CEP as allied health, reimbursement for CEPs |
| Why is reimbursement important for CEPs | most insurances do not cover the GXTs and needed info CEPs can provide on how ex can be health beneficial, so a lot of people cannot be referred to CEPs |
| Why are legal considerations important for CEPs | scope of practice varies largely across states, so what they can/cannot do opens up legal problems |
| What is the CREP | coalition for registration of exercise professionals |
| What is promotion | use of behavioral strategies in assessing and counseling individuals about their physical activity behavior characteristics |
| What is the point of behavioral strategies | to be used with supportive social and physical environments |
| What is human behavior, especially physical activity, shaped by | its surroundings |
| 4 main psychological goals a CEP should focus on during activity promotion | understanding environment, understanding physical/social contexts, addressing barriers, providing insight on overcoming barriers |
| Two most common barriers to physical activity participation | self efficacy, social support |
| What is self efficacy | a person’s confidence to be able to ex under diff circumstances |
| How is self efficacy associated with activity | positive association, more self efficacy leads to increase in participation |
| How does social support affect activity | positive, increase support increased physical activity |
| Some examples of how a physical environment can be a barrier | climate if its super hot all the time or always raining, what does/doesn’t the client have access to i.e. lack of sidewalks or bike trails or gyms far away/not present, neighborhood unsafe etc. |
| What is lifestyle based physical activity focused on | less planned exercise and physical activity, more incorporation as apart of daily routine i.e. park further, stairs instead of elevator, walk to work instead of drive |
| Why is lifestyle focus important | most common barrier is lack of time in the day |
| Premise of the health belief model | personal beliefs or perceptions will influence health behavior |
| 4 components of health belief model | perceived seriousness, perceived susceptibility, perceived benefits of change, perceived barriers of change |
| What is the most predictive construct of behavior change | perceived barriers to change |
| What has to occur for changes to be made to lifestyle | patient must think/know that benefits outweigh barriers |
| What is perceived seriousness | How severe is the disease if I were to contract it? |
| What is perceived susceptibility | How likely is it that I will contract this disease? |
| What is perceived benefits of change | Personal opinion of the value or usefulness of a new behavior to decrease risk of acquiring disease |
| What is perceived barriers to change | Personal opinion of obstacles in the way of adopting a new behavior |
| What are the 6 stages of the transtheoretical model/stages of change | precontemplation, contemplation, preparation, action, maintenance, termination |
| Precontemplation is defined by | no awareness or intention to change behavior |
| Contemplation is defined by | aware of need for change + planning for it but not committed |
| Preparation is defined by | beginning to plan change, committed to following through |
| Action is defined by | implemented behavior changes |
| Maintenance is defined by | maintaining changes and prevent termination |
| Termination is defined by | failure to maintain changes |
| What is the premise of the ecological perspective | most effective interventions occur across multiple levels, both intrapersonal and environmentally |
| 5 levels of the ecological perspective | intrapersonal, interpersonal, institutional, community, public policy |
| Intrapersonal level | within the subject, psychological and biological variables and behaviors |
| Interpersonal levels | social groups, outside support from friends, coworkers, significant others, etc. |
| Institutional levels | organizations like health care facilities, schools, companies etc. i.e. how some companies have free gym memberships to promote activity in a sedentary job |
| Community levels | networks within a defined area |
| Public policy | laws at local, state, and national levels |
| What is education focused on when it comes to physical activity | designed outcomes and understanding |
| What should patients understand about designed outcomes | reasons for referrals and what we are forming an Rx for |
| What should CEPs help patients understand about physical activity | both the fitness and health benefits of being active |
| What is the goals of the general interview | reason for referral and to form a confidential baseline for ex rx |
| 7 topics of the general interview | reason for feral, demographic info, history of present illness (HPI), current meds/allergies, past medical history, family history, social history |
| Demographics we focus on in GI | age, sex, ethnicity |
| Why is age important | survival predictor in CV+R conditions |
| Why is sex and ethnicity important | differences in onset |
| What is an example of a disease with sex differences | osteopenia + rheumatoid arthritis in postmenopausal women due to estrogen depletion |
| What is HPI | history of present illness |
| What should we be looking for in HPI | any information that led to the referral, including the chief complaint and manifestations in symptoms |
| Different in objective vs subjective in HPI | objective is present in medical record and shows in signs, subjective comes directly from the patient especially when it comes to symptoms |
| How do we characterize symptoms in HPI | OPQRSTA |
| O in OPQRSTA | onset |
| P in OPQRSTA | provocation/palliation |
| Q in OPQRSTA | quality |
| R in OPQRSTA | region/radiation |
| S in OPQRSTA | severity |
| T in OPQRSTA | timing |
| A in OPQRSTA | associated s/s |
| Onset | when did the s/s of the chief compliant start and how? |
| Provocation/Palliation | when does chief symptom increase/decrease, are there triggers? |
| Quality | verbs describing the type of pain i.e. sharp, dull, numb |
| Region/Radiation | specific location of pain, does it move/radiate |
| Severity | scale of 1-10 |
| Time | consistency and changes since onset |
| Associated S/s | anything associated that is not the principle |
| 4 Main questions of current medications | name (especially if generic vs name brand), dosage and units, administration route/how it is taken, time and frequency it is taken |
| 2 main questions for allergies | the name of the specific allergy i.e. food vs meds vs environmental components, reactions + severity of reactions |
| Why are medications and allergies important to note (3 reasons) | drug purpose, desired/side effects, medical reconcilation |
| Drugs are not meant cause ______ _____; instead they have some sort of effect on existing responses | new functions |
| Knowing the ___ ___ of meds is important because they may affect physiological readings, ex reactions, and cause symptoms | side effects |
| What is medical reconciliation | comparing the medications a patients stakes they are taking vs. their medical records, especially when it comes to consistency and frequency |
| Meds can affect ______ | heart rate response |
| What happens to blood flow during ex | significant redistribution |
| Main organ responsible for drug metabolism | liver |
| Main organ for drug elimination | kidneys |
| Main organ(s) for drug absorption | GI tract |
| How does exercise effect medication effects in the blood | blood is shunted away from visceral organs towards muscles, which can affect drug absorption and metabolism/metabolic sites of drugs |
| What is important to note about transdermal meds | bflow increases to skin during ex, can affect pathology of meds |
| Three main focuses of medical history | musculoskeletal, neurologic, and respiratory problems |
| What type of problems do we focus on in the medical history | issues that may affect ability to ex test or train |
| Examples of musculoskeletal problems that may affect ex | lower back pain, gout (posture/walking issues), joint issues |
| Examples of neurologic problems that may affect ex | cerebrovascular diseases, stroke, dementia |
| Examples of respiratory problems that may affect ex | asthma, COPD |
| What is family history limited to | 1st degree relatives, nuclear family, parents, siblings, kids, SOMETIMES grandparents |
| Important thing to note in family history | heritable disorders, especiall CVD |
| Important things to note in social history | drugs, nutrition, sleep/snoring, leisure, ex history and habits |
| 3 other important factors during interview that can effect exrx | marital status, transportation availability, occupation+nature of occupation |
| What do we look for in general state | overall view, anything abnormal, patient complaints |
| General observation of patients looks at | comfortable or stressed/anxious, healthy or frail, nourishment status, how do they PHYSICALLY present |
| 6 main s/s of CMR | angina or pain possibly from myocardial ischemia, shortness or breath at rest or mild exertion i.e. walking to the car, dizziness/syncope, orthopnea/paroxsymal nocturnal dyspnea, ankle edema, palpitations/tachycardia |
| What is syncope | loss of consciousness |
| What is orthopnea | dyspnea at rest lying vertically only alleviated by sitting up or standing |
| What is paroxysmal nocturnal dyspnea | random bursts of shortness of breath during sleep |
| What do orthopnea/paroxysmal nocturnal dyspnea indicate | left ventricular dysfunction |
| What causes syncope | loss of brain perfusion due to issues in cardiac output |
| What do we measure in the general examination | BP, HR, Res[iratory rate |
| tachycardia | >100 bpm |
| bradycardia | <40 bpm |
| Elevated bp | sbp>120 + dbp <80 |
| Stage 1 hypertensions | sbp>130 or dbp 80-89 |
| Stage 2 hypertension | sbp>140 or dbp>90 |
| Hypertensive crisis | sbp>180 and/org dbp>120 |
| How do beta blockers affect HR | decrease RHR by 10-15 |
| tachypnea | RR > 20/min |
| bradypnea | RR<8/min |
| hypoxia | blood O2 saturation <95% |
| 7 components of general exam | general state, BP/HR/RR, body fatness, CV system, musculoskeletal system, pulmonary system, functional fitness/balance |
| 7 possible measures of body fatness | height/weight/BMI, waist-to-hip ratio circumferences, skinfolds, BIA, hydrostatic weighing, bodpod, DEXA |
| BMi is a | estimate of body fatness |
| What is the assumption of BMI | weight is proportional to height |
| BMI formula | kg/m^2 |
| Normal bmi | 18.5-24.9 |
| Obese bmi | >30 |
| Waist to hip ratio (WHR) | based on fat distribution using circumference |
| android | apple shaped |
| gynoid | pear shaped |
| Which shape is the unhealthier type | apple |
| Healthy whr | <0.86(F) or <0.95(M) |
| WHR formula | waist (cm)/hip(cm) |
| What is the skinfold assessment based on | thickness of several skinfolds across the body |
| What is the premise of skinfolds | fat levels correlate highly to total body fat |
| Where are the skinfold measurements completed | right side |
| What is bia | bioeletrical impedance analysis |
| What does a higher BF correlate with in BIA | higher resistance and impedance, so less electricity flow |
| Most accurate form of body fatness | dexa scan |
| What do we do in the pulmonary portion of the examination | auscilate (stethescope) the anterior and posterior chest surfaces for breath sounds and charactize them |
| What are we examining in the CV system portion | palpating cardiac pulse, as well as in wrist and feet, skin temp, and looking for peripheral edema |
| What does cold/clammy skin indicate | poor perfusion |
| What is the swelling of extremities a sign of | coronary heart failure |
| What are we examining during the musculoskeletal portion | gait, joints, any lower back pain |
| What are the different characterizations of gait | normal, antalgic/limping, hemiplegic, shuffling, wide, etc |
| What is hemiplegic gait a sign of | stroke |
| What are some issues we may see with joints | redness, warmth, swelling, tenderness |
| What would redness at a joint during the general exam possible indicate | arthritis |
| What are 3 examples of functional fitness tests | 6 min walk test, Time Up and Go (TUG), Short Physical Performance Battery (SPPB) |
| What is Time Up and Go often used for | older individuals |
| What can we use to assess balance | berg balance scale |
| Why is balance important to assess | potential risk for falls |
| The general exam is important for | collaboration between the CEP and referring physician to determine if ex is safe and to form a baseline for the ex as well as patient education |
| 3 general uses of a GXT | diagnostic, prognostic, therapeutic |
| Diagnostic uses of a GXT | identify abnormal responses |
| Prognostic uses of a GXT | identify future responses and effects w/ disease |
| Therapeutic uses of a GXT | impact of intervention |
| Low risk defined as | <2 CV risk factors |
| Moderate risk defined as | 2+ CV risk factors |
| High risk defined as | 1+ s/s of CMR, any history of CMR |
| Who needs a GXT | moderate and high risk individuals |
| Age risk factor criteria | >45 years(M) or >55 years(F) |
| Family history risk factor criteria | MI, coronary revascularization, sudden death, in first degree relative |
| Cigarette smoking risk factor criteria | current or <6 mon to quit or environmental exposure |
| Physical inactivity risk factor criteria | improper participation for at least 3 months |
| Obesity risk factor criteria | bmi>30, waist> 102cm/40in (M) or 88cm/35in (F) |
| Hypertension risk factor criteria | sbp>120 and/or dbp>80 on 2 separate times, OR ANTIHYPERTENSIVE MEDS |
| Dyslipidemia risk factor criteria | LDL >130 mg or HDL<40 or total cholesterol >200 lipid lowering meds |
| Diabetes risk factor criteria | fasted glucose >125 or 2hr glucose>200 or Hemoglob >6.5% |
| What is the only negative risk factor | high HDL levels |
| Criteria for negative risk factor | HDL >60 |
| 5 common interchangeable terms/types of a gxt | stress ekg, reg stress test, cardiac stress trest, GXT, s/s limited gxt |
| The purpose of a gxt is always | physician referral |
| 6 elements of a gxt | pretest considerations, appearance/quantification of symptoms (not signs, self reported from patient), test termination, rest/ex/recovery EKG abnormalities, functional capacity assessment, interpretation of findings/final summary |
| 6 components of pretest considerations | testing personnel, informed consent, general interview and examination, pretest likelihood of CHD, pretest instructions/preparation for EKG, selection of ex protocol and modality |
| Testing personnel things to think about | how many techs? (normally 1, should be 2), do we need a physician in case of an event, who interprets the initial data before it gets to the final destination |
| Who is always completing the final interpretation of test data | a physician |
| What should be included in informed consent | reason for test, the procedures, explanation of major and minor risks, and patient verbalization |
| What is important to ensure on the day of GXT when overlooking the general interview and exam | no changes in the clinical status |
| What are indications | the reasons for a GXT |
| 5 indications for a GXT | assess symptoms to help diagnosis CHD or other condition, identify future risks or prognosis/functional capacity for the future, evaluate pacemaker/hr/bp response to ex, evaluate if someone meets return to work or disability, determine the effectiveness |
| What are the 7 absolute contraindications | |
| 4 relative contraindications | left main coronary stenosis, several arterial hypertension @ rest (>200 sbp or dbp>110), tachy cardia @ rest/ marked abnormal bradycardia, uncontrolled metabolic disease/electrolyte abnormality |
| Relative vs absolute contraindication | in absolute, no activity should be done until cleared by a physician due to extremely high risk; in relative, there should be caution with proceeding if BENEFITS outweigh RISK |
| Pretest instructions for subject prep | remain in comfortable workout gear, medication information, food/water |
| What substances should be avoided pre-gxt | alcohol, cigs, weed, recreational drugs, caffeine |
| How do we prep the skin for ekg placement | no oils, minimize hair i.e. shave if needed |
| When do we alter site the standard lead electrode placement | when there is a pacemaker or ICD |
| How should we select a protocol | something repeatable and common |
| Categories of protocols we can select for gxt | steady state vs ramp i.e. increasing intensity, maximal vs submaximal |
| What should we try to match in gxts | work rate increments (in METS) to patient capabilities matching ADLs |
| Recommended gxt test duration | 8-12mins |
| Main modalities of gxt | treadmill, bike, cycle ergometer, arm ergmometer |
| Athletes should have a test that matches | specificity of training |
| Two most common protocols | balke, bruce |
| Things we monitor in appearance and quantifactions of symptoms | regular communication with a thumbs up or down, RPE, handrail use, language translation |
| BORG rpe | 6-20 |
| Borg modified rpe | 1-10 |
| When do we terminate a submaximal gxt | when a predetermined met level is met |
| When do we terminate most gxts | onset of symptoms |
| What are the scales we use for angina, dyspnea, and PVD | 1-4 |
| What are 4 resting abnormalities we may see on an EKG | left bundle branch block, right bundle branch block, premature heart contraction/pre-excitation syndrome, ST-T wave length changes (>1mm depression) |
| 4 abnormalities on EKGs seen during exercise | ST segment depression, ST segment elevation, T wave changes, arrhythmia |
| What abnormalities on an EKG causes us to stop the test immediately | ST segment elevation |
| What does ST segment depression indicate | subendocrdial ischemia |
| When are t wave changes a concern | paired w st segment changes |
| What are the 3 things we assess for functional capacity | ex duration, estimated METs, VO2max |
| How does vo2 max change with age | avg 1% per year, 10% per decade; active individuals see about ½ this decrease |
| 6 items to address when interpreting an ex test | angina status, ekg findings on ischemia, ekg findings on arrhythmia, functional capacity, hr response, bp response |
| What are we addressing with angina status | typical v. atypical v. none, time to onset, how it affected test, was it resolved |
| What are we addressing with ekg status on ischemia | is there st segment depression |
| What are we addressing with functional capacity | peak MET level compared to normal, and why we stopped |
| What are we addressing with HR and BP | before, during, after |
| What do we do if a patient cannot exercise | stress ekg w/imaging |
| Two types of stress ekgs we can complete | EKG+echocardiogram/stress echo, EKG+radionuclide imaging/nuclear stress test |
| What does a stress echo assess | wall motion abnormalities |
| What does a nuclear stress test assess | distribution of blood flow |
| How do stress ekgs mimic exercise | chemically inducing HR and BP increases |
| What is the name of the drug used in EKG stress and imaging | dobutamine |
| The brighter the glow on the nuclear means | more blood flow |
| Ex Rx does/does not require the approval of a physician | does not |
| Purpose of ex rx | provide a valid and safe ex guide for patient to improve health and physical activity |
| Common goals of ex rx | improve appearance/QOL, weight management, pre-comp, general health, decrease disease burden |
| What type of goals are we setting with ex rx | SMART goals |
| What does SMART goals stand for | specific, measurable, achievable, realistic, timely |
| Specificity principle | train for specific adaptations |
| Overload principle | magnitude of stimulus/volume of ex and benefits gained |
| Reversibility principle | if you don’t use it, you lose it |
| What does FITT stand for | frequency, intensity, time, type |
| Intensity could be measured by | vo2, HR, calories, watts, RPE |
| Type is synonymous with | mode |
| Questions to ask about specificity | specific goals (health/fitness vs performance), do you want to ex more, do you wanna do ADLs, do you wanna do something you cant |
| Questions to ask about mode | what type of ex do you like best or least, what equipment do you have access to |
| Questions to ask about intensity | how many days/week do you have available |
| Questions to ask about intensity | are your goals around health or fitness improvement, do you have any possible impairments |
| Questions to ask about time | how much time do you have a day, whats the best time, can you get up early/take a break/incorporate it somewhere else |
| Proper ex training sequence (4) | warmup, aerobic session and/or resistance training, static stretching (not ballistic) |
| General recommendations for cardiac endurance | dynamic large muscle activities, mimic ADLs |
| General recommendations for resistance | full ROM, proper breathing (out during lift, in during recovery) and form (no back arch), control the movement especially during eccentric |
| 3 types of flexibility training | static, ballistic, PNF |
| Which type of training is not recommended for clinical populations | ballistic |
| Static stretching | stretching the muscles surrounding a joint without movement |
| Proprioceptive neuromuscular facilitation (PNF) stretching | isometric contraction, relax, then stretched again |
| Ballistic stretching | rapid moving a muscle to stretch and relax quickly for several reps |
| ACSM recommendations are not | realistic |
| Summary of acsm recommendations | 3-5x a week, 20-60mins, 40-89% HRR/vo2max, moderate 40-59 or vigorous 60-89 |
| Summary of acsm recs for deconditioned | 2x a week, 10 mins a session, 40% HRR |
| Garder recommends to start with a ______ program and then ___ | doable, progress |
| Minimum program requirements | CR- 10min/bout, 2-3 times a week; Resistance- 2-3x; Flexibility/balance- as often as possible, can be done every day |
| Important things to monitor in ex | BP before during after, s/s of intolerance, and partner training |
| What is diabetes mellitus | a group of metabolic diseases |
| What is diabetes characterized by | inability to produce sufficient insulin OR inability of insulin to function properly |
| What is the result of diabetes | hyperglycemia, elevated blood sugar |
| What are the reasons diabetes is becoming an epidemic | increase overweight/obesity, ore sedentary lifestyles, poor eating practices |
| Where does insulin come from | beta cells in the islets of langerhans |
| What is the main organ associated with insulin production | the pancreases |
| What is the function of insulin | promoting tissues to remove and store glucose from the blood, as well as amino acids and fats |
| What is the main mechanism of t1d | lack of insulin production, so there is nothing to regulate blood sugar |
| What is the main mechanism of t2d | insulin is produced in smaller amts, remaining amts are not accepted and do not function properly so blood sugar cannot be properly regulated |
| What type of diabetes is preventable | t2d |
| Type types of t1d | immune mediated/juvenile onset, idiopathic |
| What causes immune mediated/juvenile onset t1d | beta cells that create insulin are destroyed because they are wrongly targeted by immune system, leads to insulin deficiency |
| What type of diabetes is considered an autoimmune disease | t1 immune mediated/juveline onset |
| What causes idiopathic t1d | unknown |
| When does idiopathic t1d occur | anytime |
| What is the cause of t2d | multifactorial, combo of genetic predisposition and poor lifestyle choices |
| What are the 2 causes in t2d | peripheral tissue becomes less sensitive and eventually resistant, beta cells decline in function leading to a loss of insulin secretion |
| Why is t2d no longer adult onset | children have been developing t2 because of diabetes |
| What is the most common form of diabetes | t2 |
| What is the temporary type of diabetes | gestational diabetes mellitus |
| when/how is gestational diabetes diagnosed | 2nd/3rd trimester via oral glucose challenge |
| Gestational diabetes has an increased risk of | t2d |
| What is the primary issue in diabetes | hyperglycemia |
| Uncontrolled diabetes is characterized by | being above the patients glycemic goal |
| s/s of uncontrolled diabetes | dehydration, polyuria, headache, weakness, fatigue |
| How can uncontrolled diabetes be treated/managed | hydration, bsugar monitoring, meds |
| What can happen if diabetes is not controlled | diabetic ketoacidosis, hyperosmolar nonketotic syndrome |
| What is diabetic ketoacidosis | poor control that leads to the formation of ketones from ineffective fat metabolism |
| What is a ketone | chemical byproduct from fat breakdown that causes an increase in blood acidosis |
| Which type is more prone to ketoacidosis | t1 |
| What is hyperosmolar nonketotic syndrome | a prolonged state of hyperglycemia due to illness/stress/no diagnosis |
| What are the s/s of Hyperosmolar nonketotic syndrome | severe dehydration, decreased mentation, possible coma |
| What type is Hyperosmolar nonketotic syndrome more common in | t2 |
| What is the secondary important complication of diabetes | hypoglycemia |
| What causes hypoglycemia | too much insulin, too little carbs, missed meals, excessive ex |
| What are the 3 levels of complications | macrovascular, microvascular, neuropathy |
| What are macrovascular complications | disease in large vessels that supply the coronary arteries, cerebrum, and peripheries that leads to symptoms of PAD like IC and ex intolerance |
| What are the microvascular complications | disease in smaller vessels that supply the eyes and kidneys |
| What is the effects of microvascular complications | blindness, renal failure |
| What are the peripheral neuropathic complications | loss of sense in periphery especially hands and feet |
| What are the autonomic neuropathic complications | nerve damage that disrupts the ANS regulation of the systems i.e. abnormal HR, BP, etc |
| Why are diabetics are high risk for amputations | multifactorial limb dysfunction |
| s/s of diabetes | polydipsia, polyuria, weird weight loss, slow healing, blurry vision, fatigue |
| Important things needed in the med history for diabetics | ex history, bw/bmi, blood sugar/nutrient/hemoglobin values, any other issues |
| What should we look for in the physical exam for diabetics | poor eyesight, neuropathy, limb dysfunction/issues |
| 3 criteria for prediabetes prediagnosis | fasted b.s around 5,6-6.9mmol, two-hour bs 7.7-11.0mmol, a1c 5.7-6.4% |
| What is IFG | impaired fasting glucose |
| What is IGT | impaired glucose tolerance |
| What is characterized by IFC and IGT | pre-diabetes |
| 3 criteria for diabetes diangosis | fasted bs >7mmol, two hr glucose >11.1, a1c>6.5 |
| 5 main forms of treatment for diabetes | exercise, medical nutrition therapy (MNT), self monitor blood sugar, diabetes self management education, medication |
| What does MNT focus on for diabetes | weight loss from meal replacement or bariatric surgery, only for extreme cases |
| Who can deliver diabetes self management education | a certified diabetes educator, seperate certification |
| Blood glucose goals for diabetics | fast 4.4<x<7.2, 2hr post <10, a1c<6.5-7% |
| When is ex testing necessary for diabetics | when they are not well controlled and have other major risk factors |
| When is ex testing not necessary for diabetics | when they have it well-controlled and no other major risk factors |
| When is ex testing beneficial for diabetics | when vigorous training is planned or to develop a baseline for exrx |
| What is the recommended ex testing mode for diabetes | treadmill or ergometer |
| What should a CEP ask a diabetic about prior to ex testing or training | glucose levels, food intake, medications |
| How can chronic complications influence a diabetics gxt | heart/peripheral disease can affect peripheral neuropathy i.e. decreased flow and feeling in limbs; can also decrease BP HR and redistribute blood flow |
| Acute benefits of ex for diabetics | improve bsugar levels, more glucose control, better skeletal muscle use of glucose to decrease plasma glucose |
| Chronic benefits of ex for diabetics | improved metabolic control, reduce hypertension, better bloop lipid, weight loss/management, prevention of t2d, psychological |
| Why is consistency important when exercising with diabetes | insulin effects are loss if not training is not consistent |
| Definition of obesity | excessive fat accumulation that is a risk to health |
| How is obesity rated | using bmi |
| When do most obesity occurences occur | 70 percent in adulthood |
| 5 factors that affect obesity | decreased physical activity, increased food intake, societal influence, individual psychology, biology |
| In regards to energy, obesity is the result of | longstanding energy imbalance/positive energy balance, where More calories are consumed than expended over a long period of time |
| Obesity increases the risk of | every comorbidity |
| s/s of of obesity | fatigue, dyspnea, physical activity difficulty |
| What should you do at every visit with an obese patient | review physical factors, assess ex history and progress |
| What is important to determine with obese patients before continuing with gxt and ex rx | their readiness to change in the transtheoretical/stages of change model (based on 6 month blocks) |
| 5 general treatments for obese patients | diet therapy, behavioral therapy, exercise, pharmacotherapy, surgical |
| What is surgery reserved for | severely obese patients |
| What is the treatment goal for obese patients | bmi>25 |
| Common percentage goal for obese patients | 35% of current weight |
| What is important ot consider when developing obese patient goals | SMART goals, especially with timeline and expectations, remain realistic |
| When should obese patients go to a more intensive strategy | any CV risk factors or a CMR, weight loss failure, >25 lb/10% goal loss |
| When is meal replacement and pharmaco therapy introduced | bmi>30 |
| What is the basis of diet therapy | calorie reduction based on RMR and physical activity |
| What is needed for 1 lb of fat weight loss | -3500 deficit |
| Hypocaloric diet | extreme diet with only 500-750 kcal/day |
| Two types of meal replacement diets | partial or complete |
| Complete meal replacement is also | very low calorie diet, VLCD |
| What is the goal of behavior therapy for the obese | using behavior change theories to promote exercise adherence |
| Four theories/practices used for obese behavioral therapy | stages of change, cognitive restructuring, individual/group therapy, lapse/relapse planning |
| What is cognitive restructuring | changing the way someone thinks about ex to avoid an all or nothing success or fail mindset based on strict numbers |
| Weight loss is fastest in individuals when | combined with diet and exercise behavior change |
| Weight loss drugs are recommended for what bmi | >30 |
| Most common weight loss drug | glp1 agonists |
| Two types of glp1 agonists | ozempic/wegovy/semaglutides, zepbound/tirzepatide |
| What is the fastest growing area of obesity treatment | surgery |
| Restrictive effect of surgery | stomach size reduction |
| Malabsorptive effect of surgery | changing the GI to absorb fewer calories (gastric bypass) |
| What is/are metabolic syndromes | a collection of interrelated cv/m risk factors that are present in a person more frequent than expected |
| Most common demographic of metabolic disease | obese individuals |
| What risk is increased w/ metabolic syndrome | atherosclerotic CV disease |
| Issues that combine and cause metabolic syndrome | obesity/abdominal adiposity, insulin resistance, mitochondrial dysfunction |
| 5 components of metabolic syndrome | abdominal obesity, high fasted glucose, low HDL levels, hypertension, high triglycerides |
| What does metabolic syndrome normally lead to | t2d and ascvd |
| Triglyceride criteria for metabolic syndrome | >150 |
| BP for metabolic syndrome | SBP>130 or DBP>85 |
| Blood glucose criteria for metabolic syndrome | >100 |
| How many of the component criterias reflect metabolic syndrome | 3+ |
| Main treatment goals for metabolic syndrome | similar to obesity, weight loss, physical activity, improve diet, medications, or surgery |
| Is ex testing needed for obesity | no |
| Is ex testing needed for metabolic syndrome | no |
| What do we do when testing an obese individual w/ difficult walking | different mode |
| Goal for ex rx for obesity/ms | 2000+ kcal expended/week, combining aerobic and resistance to prevent sarcopenia |
| When should we focus on balance with obese ex rx | extreme weight loss due to a shift in center of gravity |
| What is important for successful weight management | a multifactoral approach |
| What should not be underestimated as an CEP when trying to develop programming and educate obese patients | psychology, especially behavior therapy |
| 3 layers of the myocardium | epicardium, myocardium, endocardium |
| How does the myocardium receive blood | coronary arties |
| What is an MI | myocardial infarction, a blockage in coronary blood flow resulting in cell damage |
| How does ex training affect MI | protects against heart damage |
| What is hematocrit | percent of blood composed by RBCs |
| 4 components of blood | plasma, rbcs, wbcs, platelets |
| What % of blood is hematocrit | 42 |
| Formula for MAP | DBP+0.33(SBP-DBP) |
| How does the pns regulate the heart | via the vagus nerve, slow HR via SA/AV inhibition |
| What happens with a decrease in parasympathetic tone | HR increase |
| What causes increase in HR at ex start | parasympathetic withdrawal, then SNS simulation |
| What is heart rate variability | time between heart beats, should be wide |
| What does low HRV mean | low mortality |
| What is edv | end diastolic volume, volume of blood in ventricles at end of diastole/preload |
| What is the frank starling mechanism | increase edv means bigger contraction |
| What is edv dependent on | venous return |
| How is venous return increased | venoconstriction, skeletal muscle pump |
| How is sv regulated | edv, avg aortic bp, contracility |
| What increases co | increases hr and sv |
| At the same o2 uptake, ___ work causes higher hr and bp | arms |
| What 4 diseases are included in cvd | CHD, heart failure, hypertension, stroke |
| What is the leading cause of death in the US | CVD |
| What % of cvd deaths are from chd | 50 |
| CHD is caused by | acute coronary syndromes (ACS) |
| 3 diseases of ACS | unstable angina pectoris/chest pain, acute myocardial infarction/heart attack, potentially sudden cardiac death |
| What causes chest pain | ischemia |
| What is ischemia | decreased blood flow/oxygen |
| What is an acute MI | death of cardiac muscle cells due to prolonged ischemia |
| What time of ___ causes acute MI | occlusion; 60+ mins |
| What is potentially sudden cardiac death | abrupt loss of heart function from electrical disturbances, normally triggered by an MI |
| 4 layers of the artery | endothelium, intima, media, adventitia |
| What layer is where athersclerotic lesions are formed | intima |
| What is atherogenesis | disease process that results in lesions that limit blood flow in important vessels |
| What are the 5 main vessels affected in atherogenesis | epicardial coronary, carotid, iliac, femoral arteries, aorta |
| 4 steps in the pathophysiology of atherogenesis | endothelial injury, inflammatory response, endothelial dysfunction, plaque formation |
| In atherogenesis endothelial injury is ___ and/or ____ | chronic, excessive |
| What are 5 causes endothelial injury | LDL cholesterol, hypertension, glycated substances (side effect of diabetic hyperglycemia), infectious agents, tobacco smoke/irritants |
| What is the inflammatory response of atherogenesis | a product of chronic/excessive injury |
| Components of the inflammatory response in atherogenes | platelet aggregation, monocyte accumulation, LDL/foam cell accumulation |
| What causes endothelial dysfunction | chronic endothelial injury |
| 3 mechanisms of endothelial dysfunction | increased adhessiveness of platelets/monocytes to artery, increase lipoprotein permeability, impaired vasodilation/increased vasospasm |
| How do plaques form in atherogenesis | platelets cause the growth, lesion starts at intima and goes to other layers that causes a narrowing of the lumen |
| Physical description of plaque | firm, pale gray plaque and a fibrous cap |
| How does atherogensis progression vary | based on size/volume of lesions and its stability |
| Why is there a risk of embolus in atherogenesis | plaque rupture of fibrous cap can dislodge and cause obstruction |
| How do we diagnose acute coronary syndromes | via clinical assessments |
| What do we look for in ACS clin. assessment | symptoms history, a painless MI, dyspnea (labored breathing), and atypical symptoms |
| Things to look for in the physical exam for ACS | bp variations, diaphoresis, sinus tachycardia @ rest, tachypnea, heart murmurs, lung crackling |
| What is diaphoresis | excessive sweating |
| What is tachypnea | rapid breathing |
| 4 testing mechanisms for ACS | ekg, echocardiogram, chest xray, lab results |
| What manifests on an EKG that indicates ACS | ST elevation/STEMi, T wave abnormalities |
| Echos can show | area of heart damage |
| Chest xrays can show | heart size and pulmonary edema |
| Lab results can show the presence of ___ in ACS | cardiac troponin cTn |
| What do elevated cTn levels indicate | heart muscle is damaged, likely NSTEMI or STEMI |
| Two classifications of an acute MI | NSTEMI, STEMI |
| NSTEMI vs STEMI | one has st elevation, one does not; NSTEMI is only partial and less damage |
| Triad variables of acute mi | >30 min chest pain, ST seg/T wave changes on EKG, biomarkers of myocyte necrosis (cTn) |
| How many variables are needed for acute MI diagnosis | 2 of 3 |
| STEMI is classified by | extensive damage from a completely occluded coronary artery |
| NSTEMi is classified by | less damage due to clot dissolution |
| Most common treatments for acs, especially most MI | antiplatelets, beta blockers, ace inhibitors, statin |
| What is a non-medication treatment for acs | reperfusion therapy |
| Two types of reperfusion therapy | percutaneous coronary intervention/coronary catheterization, coronary artery bypass graft surgery (CABG) |
| What are the 4 factors associated w/ poor prognosis | LVEF <35 percent or CHF, <5 met ex capacity, proof of bad ischemia during ex/pharmacy testing, complications like renal failure or stroke |
| What is CHF | congestive heart failure |
| What is lvef | left ventricle ejection fraction |
| Benefits for ex testing after MI | evaluate s/s and ischemia, determine need for angiography, effectiveness of meda, assess the future, determine ex capacity |
| What bp has bad prognosis | failure of SBP to increase >10mm |
| 3 locations for ex rx for acs | inpatient rehab, initial home rx, outpatient cardiac rehab |
| What are the goals of inpatient rehab | 2-3 days to discharge, get mobile and active asap, prevent a 2nd coronary episode |
| In inpatient rehab, how is 2ndary coronary prevention promoted | med adherence, diet, ex, stop smoking |
| What should intensity be for acs patients | below the ischemic threshold (where ischemia comes on) via using RPE instead of HRR |
| What should be an extra focus of acs patients | chest stretching post open heart surgery |
| What is the 3 purposes of heart revascularization | restore myocardial bflow, symptom reflief, improve life prognosis |
| 4 heart revascularization procedures | angiography, percutaneous transluminal coronary angioplasty (PTCA), stent therapy, coronary artery bypass surgery (CABG) |
| What is a coronary angiography | a catheter is inserted in leg up to aorta, stops at LCA, put in a contrast agent to show location of stenosis |
| What is a PTCA | revascularization completed by inserting a catheter to the site of the coronary lesion to compress, redistribute, or remove plaque |
| 3 types of ptca’s | balloon angioplasty, atherectomy, laser angioplasty |
| Balloon angioplasty | balloon catheter inflated to stretch vessel and increase diameter |
| atherectomy | plaque removal via a blade catheter |
| Laser angioplasty | beam used to vaporize plaque into water+gas |
| PTCAs are recommended for people who (2) | 1-2 vessels, especially coronary, that are narrowed/blocked; Ejection Fraction equal to or greater than 55% |
| Why is ejection fraction around 55% and <2 vessels recommended PTCA | less severe damage, so less invasive surgery compared to CABG to restore function |
| What is stent therapy | revascularization by reducing acute closures, restenosis of coronary arteries after PTCA |
| What should precede stent therapy | a ptca |
| What is restenosis | re-narrowing of an artery after it has been treated |
| What causes restenosis | scar tissue or rebuilding of plaque |
| What is the old method of stents | bare metal coiled + oral anticoagulation |
| What is the new method of stents | steel mesh, drug eluting sten + oral anticoagulation meds |
| Which method of stents are latticed | new |
| What is endothelial hyperplasia | overgrowth of endothelial/muscle tissues inside an artery where a stent was placed |
| What causes endothelial hyperplasia | over-healing response from the endothelium that causes the narrowing of the stent |
| What does endothelial hyperplasia lead to | restenosis |
| What are future stents hoping to be made of | biodegradable polymer resins |
| How do the new future stents affect restenosis | reduce endothelial hyperplasia and late stent thrombosis |
| What is late stent thrombosis | formation of a blood clot inside a stent |
| Coronary artery bypass surgery (CABG) | revascularization of the heart via a venous graft from arm/leg or an arterial graft to create a bypass (like a detour) around the damaged vessel |
| Who is cabg reserved for | ptca failure, patients who cant get an angioplasty but have vessels that can preserve left systolic function, multivessel disease not fixable by angioplasty or stenting, technically difficult lesions |
| example(s) of technically difficult lesions | on the curve, distal location |
| Order of least to most invasive surgeries | ptca, stents, cabg |
| Where do thoracotomies occur | side of chest thru the ribs |
| What is a sternotomy | surgical incision down the midline of the sternum |
| Conventional sternotomy | most invasive, open chest |
| Two types of minimal incision surgeries | right anterior thoracotomy, mini sternotomy |
| Which surgery does not require splitting the sternum | right anterior thoracotomy |
| CABG is highly | invasive |
| What is the size of the incision in a sternotomy CABG | 8-10in |
| When and what is a heart lung machine used for | cabg open sternotomy, to move blood away from the heart |
| How is the heart revascularized in a cabg | a healthy vein or artery is used to make a new path around the blocked artery |
| How is the breastbone closed | wire |
| What predicts the success rate of a revascularization procedure | severity of lesion, location of lesion, comorbidities, age |
| Post cardiac revascularization, what ex begins immediately | mobilization and cardiac rehab |
| What is the educational focus on for cardiac revasc patients | meds, home activity, following up |
| What should ex focus on once out of the hospital for cardiac revasc patients | improve cardiac performance (rest and ex), improve ex capacity, improve angine-free ex tolerance |
| How is angina free exercise tolerance increased | peripheral muscular adaptations |
| What is the primary issue with ptca | restenosis |
| What are we always looking for in ex with ptca patients | angina s/s |
| When should outpatient ex programs begin for ptca patients | post discharge |
| What are the primary concerns with exercise for cabg patients | incision healing, sternal stability (if open heart), soreness/stiffness, hypovolemia, low hemoglobin |
| What is hypovolemia | loss in blood volume post surgery |
| How does hypovolemia affect ex | decreased cardiac output |
| What causes low hemoglobin concentrations | blood loss during surgery |
| How does low hb limit ex | less o2 carrying capacity which limits exercise ability and causes faster fatigue |
| What is peripheral artery disease (PAD) | blockage of leg arteries from plaque that leads to a narrowing of arteries in the lower extremities |
| What is the result of PAD | decreased blow to leg muscles |
| What % of PAD patients have intermittent claudication | 35-40 |
| What % of PAD patients experience critical limb ischemia | 1-2 |
| Most common risk factors for pad | diabetes, smoking, hypertension, hypercholesterolemia, increased blood viscosity |
| What do pad patients have an increased risk of | CV and cerebrovascular disease |
| PAD has the same pathophysiology as | atherogenesis |
| Number one sign of pad | intermittent claudication |
| What is intermittent claudication | basically angina in leg, pain cramping aching |
| Provocation and palliation of PAD | increases with physical exertion, decrease with rest |
| Most common location of IC | calf |
| Why is the calf the most common IC location | gastrocnemius has an increase in 02 consumption during walking, but PAD cannot deliver o2 to lower extremities |
| What does IC in the thighs/butt indicate | pad in profunda femoris, more risk of critical limb ischemia |
| What is critical limb ischemia | chronic ischemia at rest from severe pad |
| Side effects of chronic limb ischemia | ischemia at rest, even when lying down, foot ulcers/sores that dont heal due to lack of blood, gangrene |
| What is gangrene | tissue necrosis |
| What does chronic limb ischemia normally lead to when untreated | amputation |
| 3 types of assessments for pad | scales, imaging, hemodynamic |
| 2 scales used to asses for pad | fontaine, rutherford |
| What is the fontaine scale | I, IIa, IIb, III, IV |
| Fontaine stage I | asyomptatic due to incomplete blood vessel obstruction |
| Fontaine stage IIa | mild claudication in limb |
| Fontaine stage IIb | moderate to severe limb claudication |
| Fontaine stage III | ischemic pain at rest in feet/beginnig of critical limb ischemia |
| Fontaine stage IV | ulcers, necrosis of limb |
| Rutherford scale | scale of 1-6 with objective criteria |
| Rutherford Category 0 | asymptomatic |
| Rutherford Category 1 | mild claufication, ankle pressure > 50 but >20 lower than resting |
| Rutherford Category 2 | more than 1 but not meeting 3 |
| Rutherford Category 3- | cant complete standard treadmill, ankle pressure <50 |
| Rutherford Category 4 | ischemic rest pain, ankle pressure <40, flat/barely there ankle pulse volume recording, transmetatarsal pressure < 30 |
| Where is transmetatarsal pressure taken | across foot, just behind toes |
| Rutherford Category 5 | minor tissue loss, nonhealing ulcers, ankle pressure <60 at rest, toe pressure <40 |
| Rutherford Category 6 | same as 5, but non salvageable foot |
| Two types of imaging for pad assessment | ct angiography, mri angiography |
| What do imaging studies provide for pad | anatomic detail |
| What is the first choiceof imaging for pad | ct angiography |
| What does ct angiography do | detailed imagine of blood vessels/tissue via an iodine contrast injection |
| Which imaging technique can be used with/without contrast | MRI angiography |
| How does mri angiography get an image | radio frequency waves to give an image of the vessels |
| Disadvantage of ct angio | ionizing radiation and nephrotoxic contrast |
| Disadvantage of mri angiography | more cost, complicated, cant be used w pacemakers, hard to see stents |
| What do hemodynamic studies show | functional info via pressure measurements |
| 4 types of hemodynamic studies used to diagnose pad | ankle-brachial index (ABI), toe pressure/toe-brachial index, segmented limb pressures, transcutaneous O2 pressure |
| What is the most common hemodynamic test to diagnose pad | ankle brachial index |
| What is the ankle brachial index | assessment of the pressure differences between the brachial artery and dorsalis pedis/posterior tibial arties using BP cuffs and a ultrasound probe |
| What are the two anatomical locations at the ankle used for the ABI | dorsalis pedis arteries, posterior tibial arteries |
| What are segmental limb pressures | bp measures at diff segments of the leg |
| What is transcutaneous o2 pressure | a skin sensor that detects o2 delivery to tissue |
| Two categories of PAD treatment | optimal medical treatment, revascularization |
| What are the components of pad optimal medical treatment | minimizing risk factors, antiplately agents, improve claudication |
| What drug is shown to improve IC | cilostazol |
| What drug could possibly improve IC | ace inhibitors |
| Two categories of vascularization techniques for pad | surgical bypass or endovascular |
| What are the 4 types of revascularization procedures for cad | the same as those treating acs, ptca, stents, atherectomy, bypass |
| ____ may persist in pad patients after treatment | claudication |
| What needs to be measured before and after testing in pad patients | ABI |
| What is the goal of ex testing in pad patients | define their functional limitations, especially walking/prosthetics |
| What are we examining with cardio testing in pad patients | is there IC, at what point in time and intensity does it appear |
| PAD ex testing protocol | treadmill at a constant 2mph, 2% grade increase every 2 mins, end at intolerance |
| What is abnormal pre/post abi for pad ex testing | ankle pressure drop by >30 or >20% of baseline, taking >3min to normalize |
| What is the alternative ex testing to the modified treadmill for pad testing | 6 min walk |
| What is the purpose of a 6min walk test for pad patients | to predict functional capacity based on distance |
| ___ percent of PAD patients cant complete treadmill walking | 16 |
| Alternative modalities for pad patients | arm/leg ergometry, recumbent stair stepping |
| low/high intensity training is beneficial for pad patients | low |
| What guides intensity ex rx for pad patients | IC symptoms |
| What type of training is preferred for pad patients | supervised |
| What should ceps focus on as intensity increases with pad patients | potential cvd symptoms due to high rates of comorbid cad |
| Benefits of ex for pad patients | increased walk distance, higher ischemic threshold/time to IC onset increases, decrease risk of CV event |
| What is the primary goal of training for pad patients | increase walking distance |
| What are the benefits of increase walking distance in pad patients | increased angiogenesis and circulation, increase blow, increase o2/substrate filtration from improved metabolism, increased pain tolerance, increased endothelial function, decreased blood viscosity and severity of atherosclerosis |
| Common age for pacemakers | >65 yrs |
| Why is the number of pacemakers growing | more elderly ppl |
| Normal pathway of an electrical conduction | SA to AV to bundle of His to right/left ventricular branches to Purkinje fibers |
| 2 main Types of cardiac electrical problems | sick sinus syndrome, AV conduction block |
| Sick sinus syndrome (SSS) | heart rhythm disorder at the SA node that causes the inability to generate a heartbeat/increase HR as a response |
| What does SSS result in | bradycardia, long HR pauses, irregular heart beats |
| Symptoms of SSS | heart palpitations, angina, fatigue, light headness, ex intolerance, syncope |
| SSS on an EKG will display | long pauses between HR, then abnormal beats |
| AV conduction block | loss of AV synchrony, more serious, same s/s as SSS |
| What is the goal of the pacemaker | regulate HR, synchronize the heart, defibrillate if there is an arrhythmia |
| Pacemakers are | pulse generators |
| 3 components of a pacemaker | metal case (circuit), lithium battery, 2-3 pacing leads, and an activity sensor on the circuit |
| Pacemaker implantation is | fast and noninvasive |
| Where are pacemakers placed | just below skin, inferior to left clavicle |
| 3 types of pacemakers | temporary external pacemakers, permanent pacemakers, AICD |
| When do we use temporary external pacemakers | in emergency or ICU cases as a temporary fix until permanent pacemaker is placed |
| Where are the pacemaker leads placed | in the superior vena cava |
| Physiological pacing | sequence and timing of contractions between atria and ventricles to overcome chronotropic incompetence |
| What is chronotropic incompetence | the inability of the heart to increase its rate appropriately during ex/stress |
| What are the two types of physiological pacing | fixed rate vs rate responsive |
| Av timing interval | signals ventricles to contract |
| Optimal av delay | how fast ventricle contracts optimally, should be 150ms from beg of atrial depolarization |
| Maximal tracking rate | highest pacing rate allowed, normally 110-150bpm |
| Single chamber | 1 lead to RA |
| When is single chamber pacing used | bradycardia without av block |
| Dual chamber | 1 lead to rv, 1 lead to ra |
| When is dual chamber pacing used | bradycardia w av block |
| Max number of letters in a pacemaker code | 5 |
| First letter of pacemaker code | chamber paced |
| 4 options for 1st pacemaker code letter | A, V, D, o |
| What does D mean in pacemaker coding | both atria and ventricle |
| What chamber side do pacemakers always regulate | right |
| 2nd letter of pacemaker code | chamber sensed |
| The 2nd letter of pacemaker code has the same options as | the first letter |
| 4 options for 3rd letter of pacemaker code | T, I, D,o |
| Third option of pacemaker code represents | how the pacemaker responds |
| What does the T in the 3rd letter of pacemaker code represent | triggered |
| What does the I in the 3rd letter of pacemaker code represent | inhibited |
| What does the D in the 3rd letter of pacemaker code represent | dual, pacemaker can trigger or inhibit |
| Fourth letter of pacemaker code | programmable features |
| 4 letter options on 4th letter of pacemaker code | P, M, R, o |
| What does the P in the 4th letter of pacemaker code represent | rate/output |
| What does the M in the 4th letter of pacemaker code represent | multiprogrammable |
| What does the R in the 4th letter of pacemaker code represent | rate responsive |
| Fifth letter of pacemaker code | multisite pacing/dual function |
| 4 letter options on 5th letter of pacemaker code | P, S, D, o |
| What does the P in the 5th letter of pacemaker code represent | pacing |
| What does the S in the 5th letter of pacemaker code represent | shock |
| What does the D in the 5th letter of pacemaker code represent | dual, both pacing and shock |
| Ex testing with a pacemakers requires _____ for optimal functional response | adjustment |
| For pacemaker patients, ex testing determines | anginal threshold |
| Formal ex testing for pacemaker | bruce protocol |
| Informal ex testing for pacemaker | Chronotropic assessment exercise protocol |
| What is a Chronotropic assessment exercise protocol | a stress test to evaluate hr increase, can just be a modified bruce to monitor hr |
| Why is it important to know about the type of pacemaker | fixed rate operates differently than rate responsive |
| Difference between fixed rate vs rate reactive | fixed rate fires at one constant hr and does not adjust, stressing SV during ex; rate response fluctuates based on body sensors that detect activity and adjust properly |
| What should you expect to happen to hr with a fixed rate hr | stay the same |
| What can happen with abrupt hr decreases and pacemakers | side effects of a quick drop like dizziness, lightheadness, fall risk |
| Type of rate responsive sensor can cause variations based on | mode |
| What type of modes cannot be used in ex rx | contact sports because there is a risk of direct pacemaker contact |
| What is an AICD | automatic internal cardioverter defibrillator |
| Who gets an AICD | high risk candidates with high MI risk from previous event |
| How is an AICD different from a standard pacemaker | includes a shock when life threatening arrhythmia is there |
| What do you need to avoid with an AICD | threshold hr that would cause a shock |
| How should we adjust hr for aicd patients | train at least 20 bpm below preset shock hr |
| COPD | a disease characterized by the presence of airflow obstruction from either chronic bronchitis or emphysema |
| Two main components of copd | chronic bronchitis, emphysema |
| What is chronic bronchitis | the presence of a productive cough, most days, 3 consecutive months in each of 2 years |
| Emphysema is | a pathological/anatomical diagnosis marked by 1, permanent enlargement of the respiratory bronchioles/alveoli and 2, destruction of the lung parenchyma w/out obvious fibrosis |
| Two defining factors of emphysema | permanent bronchiole/alveoli enlargement, lung parenchyma destruction |
| What happens to bronchioles in copd | lose their shape and become clogged w mucus |
| What happens to the alveoli walls in copd | become destroyed, decrease alveoli number but increases their size |
| Most common copd sign | cachexia |
| What is cachexia | a substantial loss of muscle mass and strength |
| 3 main causes of copd | smoking, environment, Alpha-1antitrypsin deficiency |
| What percent of copd cases are from cigarette smoking | 85-90 |
| How can the environment cause copd | long term exposure to pollutants |
| What is the genetic deficiency that causes copd | alpha-1 antitrypsin deficiency |
| Pathophysio of chronic bronchitis | excessive cough and phlegm, enlarged bronchioles, obstructed airflow from mucus and inflammation |
| What happens to smooth muscle with chronic bronchitis | smooth muscle hypertrophy |
| 7 mechanisms of emphysema pathophysiology | alveoli lose parenchymal tethering, loss of lung elasticity/recoil, reduced expiratory airflow, increased work to breathe, lungs hyperinflated, flattened diaphragm, barrel chest |
| What happens when alveoli lose parenchymal tethering | they collapse |
| Why do lungs hyperinflate | air gets stuck, dead air |
| Why does the diaphragm flatten | lungs hyperinflate and press against the diaphragm |
| Why does barrel chest occur | lungs are hyperinflated permanently and push out against the ribs |
| Chronic bronchitis and emphysema have ___ causes | similar |
| Why does the lumen of the airways become obstructed | mucus hypersecretion |
| How do we clinically test lung function | spirometry |
| What does spirometry measure | airflow over time during respiratory maneuvers |
| What do we compare copd values with | predicted normal values based on age and sex |
| How is fev1 affected in copd | FEV1/forced expiratory volume in one second is reduced |
| What is fev1 a predictor of | survival |
| How is the forced vital capacity (FVC) affected in copd | reduced |
| How is total lung capacity (TLC) affected in copd | increased |
| How does the flow volume tracings of a copd patient compared | significantl reduced inspiratory and expiratory values |
| 5 common comorbidities of copd | hypoxemia/hypercapnia, cvd, limb muscle atrophy/muscle contractile dysfunction, physical inactivity/deconditioning, malnutrition |
| s/s of copd | cough, pus mucus production, dyspnea, fever, wheezing |
| What history of pack years suggest copd | 70+ |
| What is a pack year | x amount of packs a day/years been smoking |
| What are the most common measurement to assess presence and severity of copd | lung volume measurements fev1, fvc, fev1/fv, tlc |
| What are other ways to assess copd | arterial blood gasses, chest xray, computed tomography |
| What branch of copd will show in a chest xray | emphysema, enlarged lungs |
| What comorbidities affect ex testing with copd | frailty, inactivity, cv disease, malnutrition |
| What happens with exercise for copd patients | abnormal responses |
| What shows as decreased in copd patients | peak work rate, o2 consumption, hr, ventilation; ventilatory reserve, arterial pO2 and o2 saturation |
| What increases in copd patients | hrr |
| What occurs at a lower work rate in copd patients | lactate threshold |
| What is absent in copd patients during ex | ventilatory threshold |
| Tests of functional capacity in copd patients | 6min walk test, sit to stand |
| Why are alternative tests of functional capacity preferred in copd patients | predictive, easier access, can use in gerontology |
| 4 main treatments for copd | smoking cessation, O2 therapy, medications, pulmonary rehab |
| How much O2 therapy increases survival rates | >15hrs |
| What is the goal of O2 therapy | arterial pO2 >60 or HgbO2 >90 |
| What is the goal of pharmacy treatment in copd | reduce symptom and complications, especially inflammation, bronchoconstriction and inflections |
| How does pulmonary rehab treat copd | decrease functional impairment to improve quality of life |
| Asthma is | a chronic inflammatory disorder |
| What causes recurrent asthma episodes | airway hyperresponsiveness that leads to airflow obstruction |
| Symptoms of asthma | wheezing, breathlessness, chest tightness, coughing |
| Most common time for asthma episodes | night or early AM |
| How are asthma episodes resolved | spontaneously or with treatment |
| Asthma episodes are ____ unlike copd | reversible |
| When does asthma normally begin | childhood |
| What populations have higher asthma incidence | innercity blacks |
| What causes the bodys predisposition to airway hyperresponsiveness | genetics and innate immunity/factors of the host |
| What promotes inflammation and how | cd4 lymphocytes, they activate eosinophils and mast cells |
| What causes airway hyperresponsiveness | environmental stimuli/pathogens or cold air |
| Acute process of asthma | inflammation causes bronchoconstriction, mucus secretion, and swelling that obstructs the airflow |
| Asthma attacks are | episodic |
| Chronic process of asthma results in (4) | damaged airway epithelium, fibrosis from collagen deposition, smooth muscle hypertrophy/hyperplasia, angiogenesis |
| What can impede asthma diagnosis | intermittent episodes i.e. not constantly occurring |
| Possible asthma attack stimuli | allergens, season rhinitis (runny nose), dust mites, smoke/fumes, cold air, exercise |
| 3 main things we use to diagnose asthma | medical history, physical chest exam/lungs, spirometry |
| What fev1 value do asthmatics display | <80 percent of predicted |
| What fev1/fvc value do asthmatics display | <65 percent predicted |
| What happens to the flow volume loop in asthmatics | altered, does not meet predicted values |
| What are the other clinical assessments of asthma | xray, phlegm production, possible other causes of symptoms like pneumonia or pneumothorax |
| What is ex testing used for in asthmatics | to assess a decline in tolerance unrelated to airflow limitation |
| What type of gxt do we use for asthmatics | symptom limited incremental test |
| What do we measure during ex test of asthmatics | HbO2 saturation, ekg, Vo2 cart |
| Contraindications for ex testing in asthmatics | acute bronchospasm, exercise induce bronchoconstriction, chest pain, elevated shortness of breath, severe deconditioning, orthopedic limits |
| Asthma treatment is focused on | prevention of future episodes rather than reversal |
| How to prevent exercise induced bronchospasms | mask/scarf from cold, or medications BEFORE EXERCISE |
| Exposure to what should be minimized to prevent eib | cold hair, low humidity, air pollutants |
| What ex is better for asthmatics | intermittent ex, low-intensity sports in warm, humid air |
| Asthma is airway _____ then airway _____ | narrowing, inflammation |
| arthritis | a generic term for conditions that involve inflammation of 1+ joints |
| How many different forms of arthritis are there | 100+ |
| What characterized the diff types of arthritis | various degrees of joint damage, movement restriction, functional limits, and pain |
| 3 main branches of arthritis | osteoarthritis, rheumatoid arthritis, ankylosing spondylitis |
| What is the leading cause of disability in the US | arthritis |
| How does arthritis affect social functioning | isolation, stress, depression, decreased QOL |
| What is the most common form of arthritis | osteoarthritis |
| What is most affected by osteoarthritis | hands, feet, spine, weight bearing joints |
| What is the secondary issue of osteoarthritis | loss of strength due to reduced movement |
| Osteoarthritis is characterized by | continuous abnormal remodeling of joint tissues |
| What does osteoarthritis result in | loss of cartilage, bone on bone, periarticular muscle loss, strained/weak ligaments, pain |
| Osteoarthritis leads to decreased ____ because of decreased movement | strength |
| What does bone on bone lead to | inflammation |
| What is periarticular muscle loss | muscle atrophy around ligaments |
| 6 steps of osteoarthritis | cartilage becomes damaged/rough, bone thickens to reduce load, synovial membrane swells + increase fluid, ligaments thicken, joint space narrows, cartilage is lost w/ bone on bone inflammation and ligaments are weak |
| Bone spurs form in | osteoarthritis |
| Rheumatoid arthritis | a chronic autoimmune disorder that leads to systemic inflammation and symmetrical polyarthritis |
| What is symmetrical polyarthritis | affecting joints, 2 on each side and symmetrical |
| Who is systemic arthritis more common in | women |
| What is the principal target of rheumatoid arthritis | synovial joints |
| What is synovitis | inflammation of the synovial joint |
| Effects of rheumatoid arthritis | muscle loss, increase fat, fatigue, cvd and md, t2d, osteoporosis |
| 5 steps in the process of rheumatoid arthritis | chronic immune dysfunction that attacks tissue and joints, synovitis from excess fluid + synovial cell hyperplasia (overgrowth), pannus, cartilage/bone erosion, joint destruction and ankylosis |
| What is pannus | abnormal tissue layers over the joint |
| What is ankylosis | the stifferning of the joints that restricts movement |
| Which type of arthritis is more wear and tear | oa |
| Which type of arthritis is asymmetric | oa |
| Which type of arthritis occurs more often in younger populations | ra |
| Which type of arthritis has obvious inflammation | ra |
| What is ankylosing spondylitis | chronic autoimmune disorder that effects the spine and sacroiliac joint, as well as synovitis in peripheral joints |
| What gender is AS more common | men |
| Process of ankylosing spondylitis | chronic autoimmune, lower spine ligament inflammation, bone spurs within ligaments, bridge formation between vertebrae that leads to fusion, lower back pain and immobility |
| Where are bone spurs most common | AS and OA |
| What does arthritis have secondary effects on | exercise tolerance, strength, endurance, aerobic capacity, ROM, biomechanics, proprioception, social functioning |
| 3 stages of arthritis | acute/mild, chronic/moderate, severe |
| Acute arthritis | reversible s/s |
| Chronic arthritis | stable but irreversible structural damage |
| Severe arthritis | increased pain, decrease ROM and function |
| s/s with related joints | pain, stiffness,effusion, joint locking, synovitis, deformity, crepitus, bone spurs |
| What is effusion | water/fluid around the joint |
| What is crepitus | abnormal popping/cracking |
| What is synovitis | inflammation of synovial joint membrane |
| Is there a genetic component of arthritis | yes |
| What can be useful to diagnose specific type of arthritis | extra articular features |
| Examples of extra articular features | redness, swelling, pain, heat |
| What is the test/marker for arthritis | none exists |
| What can help in arthritis type differentiation | serum/synovial fluid tests |
| What tests can assess severity and abnormalities | joint imaging, mri, ultrasound |
| What type of arthritis is at risk for cvd | ra |
| What type of arthritic individuals are at risk for CMR disease | sedentary |
| ______ and _____ testing can be performed to make a baseline for ex rx change | musculoskeletal, ROM |
| How should intensity be done in arthritis | small increases |
| When should treadmill be used in arthritis | minimal to mild joint impairment |
| When should cycle ergo be used in arthritis | mild/moderate lower extremity joint impairment |
| When should arm ergo be used in arthritis | severe lower extremity impairment |
| What is the main emphasis of arthritis treatment | emphasizing both ex and medication to control disease |
| 4 main goals of arthritis treatment | promote activity, control symptoms/improve function, healthy body comp, reduce comorbid risk |
| Non pharmacologic treatments for arthritis | education, pt/ot, braces/bandages, canes/walk aids, shoe mods/orthotics, ice/heat, weight loss, avoid repeat motion jobs, joint irrigation/surgery |
| What do pharmacy treatments vary based on for arthritis | severity and form |
| Most common meds for arthritis | NSAIDs, analgesics, corticosteroids |
| What are DMARDs | disease modfying antirheumatic drugs |
| What do DMARDs treat | RA and AS |
| Main ex rx goals for arthritis | maintain physical function, improve body comp/weight, reduce inflammation/pain, prevent contractures and deformities |
| Ex rx for arthritis should avoid ____ ____ | high impact |
| What time of day should ex avoid in arthritis | morning stiffness or the cold |
| Why do some patients avoid water with arthritis | chlroine can cause rash/inflammation |
| How does footwear/orthotics help | more support to perform adls |
| AS leads to ____ which may require a ___ ___ | bad posture, back brace |
| Corticosteroids are important to consider as they may cause | long term bone loss and atrophy because of cortisol mimicking |
| KAATSU study showed that | lower load training with blood flow restriction leads to less joint stress |
| How did the s/s of arthritis improve in the KAATSU study | decreased inflammation via increased blood flow to problematic areas to remove and filter inflammation better |
| osteoporosis | skeletal disorder characterized by compromised bone strength that increases fracture risk |
| Criteria for osteoporosis | bone mineral density (BMD) 2.5 std dev below mean/t score -2.5 |
| osteopenia | less severe form of osteoporosis |
| Criteria for osteopenia | BMD t score between -2.5 and -1 |
| When is a majority of bone mass made | childhood |
| When is peak bone mass | 20-30 years |
| What hormone inhibits bone resorption/breakdown | estrogen |
| When does osteoporosis prevention begin | childhood |
| What influences bone development | genetics, physical activity, diet, hormone balance |
| What is bone remodeling | a naturally occurring cycle of bone resorption and bone formation |
| What is bone resorption | breakdown of bone by osteoclasts |
| What is bone formation | production/mineralization of bone by osteoblasts |
| What happens what resorption>formation | bone loss |
| s/s of osteoporosis | asymptomatic, maybe a fracture |
| Risk factors for osteoporosis | sedentary, diet, post menopausal |
| What is the biggest red flag for osteoporosis | an abnormally caused fracture |
| Signs of vertebral frx | height loss, protruding abdomen, hyperkyphosis, posture changes |
| What is hyperkyphosis | excessive rounding of upper back/thoracic spine |
| What to look for in history/exam for osteoporosis | fracture risk (FRAX), fall risk, physical state, posture |
| What is the frax | fracture risk assessment that looks at 10 year probability based on algorithms and other risk factors like glucocorticoids or history |
| What is the minimum age to use frax | 40 years |
| What is the diagnostic tool used for osteoporosis | bone mineral density |
| What method gathers bmd | dxa scan |
| What location is used for the diagnosis of osteoporosis/10 year risk | femoral hip bmd |
| What location bmd can assist diagnosis | lumbar spine |
| How does ex affect bone mass | can increase or maintain bone mass |
| What vitamins can increase bone mass or slow loss | calcium, vitamin D |
| What decreases osteoclast activity | biphosphonates |
| What hormones decrease osteoclast activity | calcitonin, estrogen |
| What increases bone turnover | parathyroid hormone |
| Contraindications of osteoporosis | there are none |
| What type of ex should be avoided with osteoporosis | high impact skeletal loading like jumping |
| Goals of osteoporosis ex rx | reduce fractures via fall prevention, reduce bone loss, promotre spine-sparing strategies aka proper form |
| What type of exercise is osteogenic | load bearing, high load, few reps |
| 4 progressions of fall prevention | reduce base support (close feet to 1 foot), shift weight, reduce support contact, change sensory input (close eyes) |
| 8 examples of fall prevention ex | heel lifts, single knee lift, alternate step march, leg extension, knee curl, sit to stand, walking, heel to toe walking |
| gerontology | study of the aging process from maturity to death |
| geriatrics | branch of clinical medicine that includes diagnosing/managing older individuals |
| Why is there a pressure on health care bc of geriatrics | costs 4-5x to expend and maintain, esp >80 |
| What causes severe functional limitations in older individuals | intrinsic aging, comorbidities, deconditioning |
| Aging increases the risk of | pretty much every comorbidity |
| Why does peak vo2 decline | max hr decline 1bpm/year, decreased avO2, deconditioning, muscle disease |
| Most common s/s of older individuals | arthritis pain, dyspnea from deconditioning or cv/lung disease |
| What should ceps look specifically at for older ppl | typical conditions of aging and medication use as well as cognition |
| In old ppl, who can begin ex without a test? What type? | healthy older adults, low to moderate intensity |
| In old ppl, who needs an ex test? | high risk or wanting to do high intensity vigorous |
| What should be tested before older ppl do resistance training | strength and ROM |
| Common pretraining evals for adults | chair stand, step ups, walking speed, tandem walk, one leg stand, functional reach, timed up and go, ROM |
| polypharmacy | taking many medications |
| Why is polypharmacy important | need to understand how meds interact and their effect on ex measures |
| What type of ex is encouraged in older individuals | group classes |
| Why are warm ups and cool downs important in older individuals | bodies take longer to reach/recover homeostasis following changes |
| How often can fall prevention ex be completed | every day |
| pediatrics | branch of medicine concerned w children and their diseases |
| children | infancy/birth to adolescence, puberty until growth stops |
| Who is not considered a clinical population | children |
| Why is aerobic fitness difficult measure in kids | increased physical activity but not a resulting in increased aerobic capacity |
| How is hr affecting in children | wider variation in response |
| How do children perceive intensity compared to adults | see it as less difficult |
| Kids have a higher/lower vo2 max | lower |
| Common diseases increasing in number in kids | t2d, hypertension, dyslipidemia, metabolic syndrome |
| What is causing increased amt of ex testing in kids | increase in obesity |
| When are ex evaluations used in kids | only if absolutely necessary |
| What is ex evaluation dependent on in kids | s/s to help diagnose or develop treatment plan |
| 6 common reasons for pediatric gxt | evaluate specific s/s that happen in ex, find abnormal ex responses in kids w/ cmr orders, especially MI and arrhythmias, assess efficiency of medical/surgical treatment, asses functional capacity, evaluate prognosis, find baseline for rehab |
| What is the goal of a kids history and physical exam | ensure testing benefits outweigh risk |
| Why do kids have problems with equipment | its designed for adults, not their body size |
| How may kids peak performance be affected | may be poor |
| What issues occur with long protocols | short attention spans, poor motivation |
| What are the 5 modifications we can make for kids ex test | safe environment, 2 testers/spotters, explain test to kid and parent, modify equipment for proper size, motivate/encourage the kid |
| What are the two primary modalities for kids | treadmill, cycle ergometer, arm only if population equipment |
| Contraindications for terminated gxt in kids | diagnostic findings have been found, s/s indicate possibility of adverse event |
| What are the three levels of training goals in kids | basic, intermediate, athletics |
| Exrx aerobic training in kids | b- movement/play, i- fitness principles/higher intensity/sports, a-structured sport training |
| Benefits of resistance training in kids | improve strength/endurance, enhance motor skills, injury protection, psychological benefits |
| Exrx resistance training in kids | b- use bw and large muscles, i- machines and overload, a- sport/multi joint specific and progressive overload |
| What is the key to proper technique | supervision |
| Exrx ROM/stretching in kids | b- static major stretch, i- static+ dynamic, a- sports specific and dynamic |
| What declines as kids age | flexibility |
| What should we use to measure intensity in kids | omni rpe |
| Kids have greater risk of | heat related illness and dehydration |
| Kids have higher/lower sweat rate | lower |
| Kids bodies cool faster/slower in water | faster |
| What is it important to consider with meds and kids | many drugs are not developed for kids, so may have different interactions and side effects |
| Who do kids rely on for meds adherence | their parents |
| Kids should be exercising | every day |
| Two types of stroke | ischemic, hemorrhagic |
| What gender has a higher stroke risk | women |
| Why do women have a higher risk of stroke | longer life, increase cvd risk w menopause |
| Ischemic stroke | loss of blow to a region caused by buildup of atherosclerotic plaque in cerebrovascular arteries |
| Most common type of stroke | ischemic |
| Process of ischemic stroke | blood flow to brain blocked by a clot formation in a vessel |
| Two categories of ischemic stroke | thrombotic, embolic |
| What occurs in a thrombotic stroke | blood clot/thrombus blocks flow of blood in brain |
| What occurs in a embolic stroke | fatty plaque or blood clot/embolism breaks away and flows to brain where it blocks an artery |
| Stroke has the same pathophysiology beginnings as | cvd and pad |
| Hemorrhagic stroke | excessive bleeding in a cerebral artery that prevents blood from flowing to brain cells down the stream |
| What type of stroke has a higher chance of death | hemorrhagic |
| Process of hemorrhagic stroke | bflow to brain blocked via a leak/rupture of vessel |
| Two types of hemorrhagic stroke | subarachnoid, intracerebral |
| Subarachnoid stroke | bleed into subarachnoid space and the meninges (tissue that covers brain) |
| What normally causes a subarchnoid stroke | an aneurysm, where the blocked vessel weakens and bursts |
| Intracerebral hemorrhage | within the brain and brain tissue, normally caused by hypertension that weakens the vessel |
| What type of hemorrhagic stroke is more common | intracerebral |
| What are the risk factors for stroke | same as cvd and pad |
| s/s of stroke | memory loss, paralysis on opposite side of body |
| s/s of right brain damage | vision issues, awakward/inappropriate |
| s/s of left brain damage | speech/language issues, extremely cautious |
| Acute stroke s/s | numbness/weakness in face arm and leg, confusion speech issues and cognitive defect, impaired bi/unilateral vision, impaired coordination/walking, headache |
| BEFAST | balance, eyes, face, arms, speech, time |
| What is the main sign iof stroke n the physical exam | hemiplegic gait |
| What is commonly presented in stroke patients | cad |
| Types of imaging used to identify stroke occlusion | ultrasounds, MRI< angiography, non contrast CT, diffusion weighted MRI |
| What is the standard for hemorrhagic stroke | noncontrast CT |
| What is the standard for ischemic stroke | diffusion weighted MRI |
| What is a diffusion weighted MRI | mri that assess restriction to movement of water molecules that are then detected by the mri and appear as white spots where there is occlusion |
| 3 types of revascularization procedures for stroke | carotid endarterectomy, mechanical thrombectomy w stenting, cerebral bypass |
| Carotid endarterectomy | surgery to remove plaque from carotid |
| Mechanical thrombectomy w stenting | physical blood cot removal then placing a stent |
| 2 types of cerebral bypass | extracranial intracranial (EC-IC) or intracranial intracranial (IC-IC) |
| ECIC cerebral bypass | outside skull artery to sinde skull artery |
| ICIC cerebral bypass | 2 arteries within brain to bypass a blocked section |
| Medication treatments for stroke | tPA (tissue plasminogen activator, Activase), anticoagulants, antiplatelets, ACE inhibitors |
| What are the supportive treatments for stroke | pt, ot, speech therapy, RD, counseling |
| Why do stroke survivors need therapy | many cannot walk, highly influence QOL |
| What is the overall goal of supportive treatment for stroke victims | restore balance, movement, coordination, and qol |
| What is an important assessment needed in stroke gxt | pre ex BP, especially hypertension, and angina as ischemic stroke normally has CAD |
| Most stroke patients need a _____ ____ to assess functional capacity | modified gxt |
| Protocol for modified gxt on stroke | self selected speed, 2 percent grade every 2 min with appropriate mode |
| How to assess strength in stroke victims | hand grip dynamometer or 10rm test |
| What does handgrip dynamometer assess in stroke victims | difference between paretic/affected and unaffected sides |
| Main goal of ex rx in stroke patients | improve functional capacity fc |
| What is the min functional capacity for independent living | 20ml/kg/min |
| What is the avg functional capacity of a stroke patient | 14.4 ml/kg/min |
| What is highly correlated with functional capacity | reduced muscle mass |
| Loss of ___ is common in stroke patients | flexibility |
| What is the overall goal with exrx in stroke patients | a comprehensive rx that addresses cv, resistance, and flexibility training |
| Movements with stroke victims should focus on | mimicking ADLS |
| Special attention should be given to ____ ___ in stroke victims | paretic limbs |
| Examples of training stroke victims can use | standing leg lifts, seated marching, knee flexion |
| How often can stroke victims practice flexibility to decrease muscle spasticity | every day |
Created by:
isabellamulet