Cardinal manifestation of coronary artery disease
Character: constricting, squeezing, burning, "heaviness"
Location: substernal, across midthorax, anteriorly; in one or both arms, shoulders; in neck cheeks, teeth; in forearms, fingers, in interscapular region
Provoked by: exercise or exertion, excitement, other forms of stress, cold weather, occurrence after meals
Systolic blood pressure decreases with exercise, may occur in patients with CVD, valvular heart disease, cardiomyopathies, aortic outflow obstruction, and serious dysrhythmias. Occasionally, those without clinically significant heart disease demonstrate exertional hypotension caused by antihypertensive therapy, prolonged strenuous exercise, and/or vasovagal responses. Exertional hypotension does correlate with myocardial ischemia, however, left ventricular dysfunction, and an increased risk of subsequent cardiac events. Seven-site: chest, midaxillary, triceps, subscapular, abdomen, suprailiac, thigh
Three-site: chest, abdomen, thigh
Three-site: chest, triceps, subscapular
Seven-site: chest, midaxillary, triceps, subscapular, abdomen, suprailiac, thigh
Three-site: triceps, suprailiac, thigh
Three-site: triceps, suprailiac, abdominal
1. Obtain resting HR and BP immediately prior to exercise in the exercise posture.
2. The client should be familiarized with the ergometers. If using a cycle ergometer, properly position the client on the ergometers (upright posture, ~25 degree bend in knee at maximal leg extension, and hands in proper position on handle bars.
3. The exercise test should begin with a 2-3 min warm-up to acquaint the client with the ergometers and prepare him or her for the exercise intensity in the first stage of the test.
4. A specific protocol should consist of 2 or 3 minute stages with appropriate increments in work rate.
5. Heart rate should be monitored at least two times during each stage, near the end of the second and third minutes of each stage. If HR is greater than 110 beats/min, steady state HR should be reached before the workload is increased.
6. BP should be monitored in the last minute of each stage and repeated (verified) in the event of a hypotensive or hypertensive response
7. RPE (using Borg or category-ratio scale) and additional rating scales should be monitored near the end of the last minute of each stage.
8. Client's appearance and symptoms should be monitored and recorded regularly.
9, The test should be terminated when the subject reaches 70% heart rate reserved. (85% age-predicted HR max), fails to conform to the exercise test protocol, experiences adverse signs or symptoms, requests to stop, or experiences an emergency situation.
10. An appropriate cool-down/recovery period should be initiated consisting of either
A. continued exercise at a work rate equivalent to that of the first stage of the exercise test protocol or lower or
b. passive cool-down if the subject experiences signs of discomfort or an emergency situation occurs.
11. All physiologic observations should be continued for at least 5 min of recovery unless abnormal responses occur, which would warrant a longer posttest surveillance period. Continue low-level exercise until HR and BP stabilize, but not necessarily until they reach preexercise levels.
Men starting in the standard "down" position (hands pointing forward and under the shoulder, back straight, head up, using the toes as the pivot point)
Women in modified "knee push-up" position (legs together, lower leg in contact with mat with ankles plantar-flexed, back straight, hands shoulder width apart, head up, using the knees as the pivotal point).
The client must raise the body by straightening the elbows and return to the "down" position, until the chin touches the mat. The stomach should not touch the mat.
For both men and women, the subject's back must be straight at all times and the subject must push up to a straight arm position
The maximal number of pushups performed consecutively without rest is counted as the score.
The test is stopped when the client strains forcibly or unable to maintain the appropriate technique within two repetitions.
Two strips of masking tape are to be placed on a mat on the floor at a distance of 12 cm apart (less than 45 yrs of age) or 8 cm apart (for clients 45 or older)
Subjects are to lie in a supine position across the tape, knees bent at 90 degrees with feet on the floor and arms extended to their sides, such that their fingertips touch the nearest strip. This is the bottom position. To reach the top position, subjects are to flex their spines to 30 degrees, reaching their hands forward until their fingers touch the second strip of tape.
A metronome is set at 40 bpm. AT the first beep, the subject begins the curl-up, reaching the top position at the second beep, returning tot he starting position at the third, top position fourth, et c.
Repetitions are counted each time the subject reaches the bottom position. The test is concluded either when he subject reaches 75 curl-UPS, or the cadence is broken.
Every subject will be allowed several practice repetitions prior to the start of the test
Drug used in pharmacologic stress testing that elicits wall motion abnormalities by increasing HR, and therefore myocardial oxygen demand. Dobutamin is infused intravenously with the dose increased gradually until the maximal dose or an endpoint is achieved. Endpoints may include new or worsening wall motion abnormalities, an adequate HR response, serious arrhythmias, angina, significant ST depression, intolerable side effects, and a. significant increase or decrease in BP. Atropine may bee given if an adequate HR is not achieved or other endpoints have not been reached at peak dobutamine dose. HR, BP, ECG, and echocardiographic images are obtained throughout the infusion of atropine. Echocardiographic images are obtained. A new or worsening wall motion abnormality constitutes a positive test for ischemia. Aka prime mover
Controls the joint motion--for example, the tricep is the agonist in a push up. Still Agonists and antagonists
Agonist muscles and antagonist muscles refer to muscles that cause or inhibit a movement.
Agonist muscles cause a movement to occur through their own contraction.  For example, the triceps brachii contracts during the up phase of a push-up (elbow extension). During the down phase of a push-up, the same triceps brachii actively controls elbow flexion while relaxing. It is still the agonist, because while resisting gravity during relaxing, the triceps brachii continues to be the prime mover, or controller, of the joint action. (Agonists are also interchangeably referred to as "prime movers," since they are the muscles considered primarily responsible for generating a specific movement. This term typically describes skeletal muscles.)
Antagonist muscles oppose a specific movement.  This controls a motion, slows it down, and returns a limb to its initial position. Antagonism is not an intrinsic property; it is a role that a muscle plays depending on the motion. If a motion is reversed, agonist and antagonist muscles switch roles. Because a flexor muscle is always a flexor, in flexion it is the agonist, and in extension it is the antagonist. Conversely, an extensor muscle is the agonist in extension and the antagonist in flexion. Using the example above of the triceps brachii during a push-up, the elbow flexor muscles are the antagonists during both the up phase and down phase of the movement.
The Krebs cycle is a complex series of chemical reactions that continues the oxidization of glucose that was started during glycolysis. Acetyl coenzyme A enters the Krebs cycle and is broken down in to carbon dioxide and hydrogen allowing more two more ATPs to be formed. However, the hydrogen produced in the Krebs cycle plus the hydrogen produced during glycolysis, left unchecked would cause cells to become too acidic (2). So hydrogen combines with two enzymes called NAD and FAD and is transported to the
Electron Transport Chain
Hydrogen is carried to the electron transport chain, another series of chemical reactions, and here it combines with oxygen to form water thus preventing acidification. This chain, which requires the presence of oxygen, also results in 34 ATPs being formed (2).
Unlike glycolysis, the Krebs cycle and electron transport chain can metabolise fat as well as carbohydrate to produce ATP. Lipolysis is the term used to describe the breakdown of fat (triglycerides) into the more basic units of glycerol and free fatty acids (2).
Before these free fatty acids can enter the Krebs cycle they must undergo a process of beta oxidation... a series of reactions to further reduce free fatty acids to acetyl coenzyme A and hydrogen. Acetyl coenzyme A can now enter the Krebs cycle and from this point on, fat metabolism follows the same path as carbohydrate metabolism (5).
So to recap, the oxidative system can produce ATP through either fat (fatty acids) or carbohydrate (glucose). The key difference is that complete combustion of a fatty acid molecule produces significantly more acetyl coenzyme A and hydrogen (and hence ATP) compared to a glucose molecule. However, because fatty acids consist of more carbon atoms than glucose, they require more oxygen for their combustion (2).
So if your body is to use fat for fuel it must have sufficient oxygen supply to meet the demands of exercise. If exercise is intense and the cardiovascular system is unable to supply cells with oxygen quickly enough, carbohydrate must be used to produce ATP. Put another way, if you run out of carbohydrate stores (as in long duration events), exercise intensity must reduce as the body switches to fat as its primary source of fuel.
Protein is thought to make only a small contribution (usually no more 5%) to energy production and is often overlooked. However, amino acids, the building blocks of protein, can be either converted into glucose or into other intermediates used by the Krebs cycle such as acetyl coenzyme A. Protein may make a more significant contribution during very prolonged activity, perhaps as much as 18% of total energy requirements (1).
The oxidative system as a whole is used primarily during rest and low-intensity exercise. At the start of exercise it takes about 90 seconds for the oxidative system to produce its maximal power output and training can help to make this transition earlier (1).
Beyond this point the Krebs cycle supplies the majority of energy requirements but slow glycolysis still makes a significant contribution. In fact, slow glycolysis is an important metabolic pathway even during events lasting several hours or more (2).
F: at least 3 days, preferably on most days of the week, depending on exercise tolerance, intensity, fitness and other health goals and types of exercise. Multiple short 1-10 min sessions may be prescribed.
I: 40-80% of exercise capacity using HRR, VO2R or VO2peak
RPE of 11-16 on Borg scale
Should be prescribed at a HR below the ischemic threshold
Time: Warm up and cool-down 5-10 mins, including static stretching, ROM, and light intensity (less than 40% VO2R, less than 64% peak HR or less than 11 RPE). Goal is 20-60 min of conditioning phase. May begin with as little as 5-10 min aerobic exercise with gradual increase of 1-5 min per session or 10-20% increase in time per week.
T: rhythmic, large muscle group activities with an emphasis on increased caloric expenditure for maintenance of a healthy body weight. Include upper and lower extremities. May include
Dual action cycle ergometers
Treadmill for walking
AIT is promising but has not been well enough studied to recommend--seems to increase improvements in these patients
Progression: no standard format--individualized to patient's tolerence
Acute mountain sickness: most common, headache, nausea, fatigue, decreased appetite, poor sleep. Severe cases: poor balance and mild swelling in the hands, feet or face. Develops within first 24 hours of exposure. Recovery in most individuals is 24-48 hours after symptoms peak. Much more likely to occur with rapid ascent to very high altitudes
High altitutude cerebral edema: potentially fatal, but uncommon. Less than 2% of individuals ascending greater than 12,000 Ft. Exacerbated, unresolved, severe AMS. Occurs in individuals who have AMS and continue to ascend.
High altitude pulmonary edema: also potentially fatal, occurs in less than 10% of those ascending 12,000 Ft. More common in those that repeatedly ascend and descend and exercise strenuously. Blue lips and nail beds may present. Crackles and rales in lungs may lead to increased susceptibility.
Sub-theory of self-determination theory
CET uses three propositions to explain how consequences affect internal motivation:
1.External events set will impact intrinsic motivation for optimally challenging activities to the extent that they influence perceived competence, within the context of Self-Determination Theory. Events that promote greater perceived competence will enhance intrinsic motivation, whereas those that diminish perceived competence will decrease intrinsic motivation (Deci & Ryan, 1985).
2.Events relevant to the initiation and regulation of behavior have three potential aspects, each with a significant function.
The informational aspect facilitates an internal perceived locus of causality and perceived competence, thus positively influencing intrinsic motivation.
The controlling aspect facilitates an external perceived locus of causality (a person's perception of the cause of success or failure), thus negatively influencing intrinsic motivation and increasing extrinsic compliance or defiance.
The amotivating aspect facilitates perceived incompetence, and undermining intrinsic motivation while promoting disinterest in the task.
The relative salience and strength of these three aspects to a person determines the functional significance of the event (Deci & Ryan, 1985).3. Personal events differ in their qualitative aspects and, like external events, can have differing functional significances. Events deemed internally informational facilitate self-determined functioning and maintain or enhance intrinsic motivation. Events deemed internally controlling events are experienced as pressure toward specific outcomes and undermine intrinsic motivation. Internally amotivating events make incompetence salient and also undermine intrinsic motivation (Deci & Ryan, 1985).
Adrenocortical insufficiency, adrenogenital syndrome, hypercacemia, thyroiditis, rheumatic disorders, collagen diseases, dermatologic disease, allergic conditions, ocular disorders, respiratory diseases, hematologic disorders, gastrointestinal diseases and liver disease among others