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Mr. and Ms.


is an individualized, comprehensive program developed by using various principles of rehabilitation medicine with the aim to maintain, restore, and increase the optimal physical, medical, psychological, social, emotional, vocational, and economic status of patients with cardiovascular disease

1) Energy conservation 2) Adaptive devices 3) Lifestyle modifications

Primary prevention: -the prevention of a cardiovascular disease from developing, even among individuals with risk factor Secondary prevention: -aimed at reducing symptoms and/or slowing the progression of cardiovascular disease -patients in this category have: 1.) impaired aerobic capacity/endurance associated with deconditioning 2.) impaired aerobic capacity/endurance associated with cardiovascular pump dysfunction or failure 3.) impaired circulation and anthropometric dimensions associated with lymphatic system disorders

-Leading health care issue in United States because of lack of activity and obesity in the place; most common cause of death and disability in United States; hospital discharges for people over the age of 65 shows an incidence of 767.9/10,000 for heart disease (p.1075, Delisas Physical Medicine & Rehabilitation) -In the Philippines, the NSO said heart disease was cited as the cause of 100,908 deaths or 21% percent of the 480,820 deaths reported from January 2009 to March 2010 (Heart disease is PH's top killer: NSO -Common in adults aging 60 and above (p.713, Braddom Physical Medicine & Rehabilitation) -More common in men than women (pre-menopausal stage)


artery disease post-myocardial infarction(MI) most common arrhythmia cognitive heart disease valvular heart disease cardiomyopathy others





the cardiac conduction system is a specialized system of muscle cells(myocytes) myocytes- facilitate in the contraction of the atria and ventricles intrinsic ability to contract is a unique feature of all cardiac muscle cells SA node- pacemaker of the heart; send signal to AV node AV node- has a special quality of delayed conduction allowing the sequential contraction of the atria, followed, after a short delay created by the AV node, by the contraction of the ventricles; signal then passes into the Bundle of His which divides further into left and right bundles. terminal branches of both conduction system carry the pulse signals that excite myocytes, causing contraction heart rate(HR)- number of beats per minute; maximum HR is determined by age and can be roughly estimated by subtracting the age of the individual in years from 220 stroke volume(SV)- is the amount of blood pumped out by a ventricle with each beat; with normal myocardial function, SV increases with exercise; SV is sensitive to postural changes, changing little in supine as it is near maximum at rest, while in erect position it increases in a curvilinear fashion until it reaches maximum cardiac output(CO)- amount of blood pumped into the aorta in one minute; is the product of HR x SV; increases with work frank starlings mechanism of the heart: states that the more that the cardiac muscle is stretched, the stronger the force of contraction


ETT -it evaluates physical work capacity and cardiovascular function -results of functional ETT are used for exercise prescriptions, setting vocational activity limits, and evaluation of effects of medications or other cardiac interventions Diagnostic ETT


ergometer upper extremity ergometer treadmills pharmacologic agents


-Being at 1.7 mph, 10% grade; increase speed & grade every 3 min. Naughton -Begin at 1.2 mph, 0% grade; increase speed & grade 3% every 2 min. Balke-Ware and Ware -Begin at constant speed of 3.3 mph, increase grade 3.5% every min.

positive ETT -positive for ischemia -indicates that there is a point at which the myocardial O2 supply is inadequate to meet the myocardial O2 demand -O2 demand>O2 supply A negative ETT -Indicates that at every tested physiological workload, there is a balance between 02 supply and demand -O2 demand=O2 supply


to determine the training HR as a measure of exercise intensity THR=(maxHR-restingHR)X% intensity+resting HR


-MI is an area of necrosis of heart muscle resulting from a sudden, absolute or relative, reduction in the coronary blood supply. -2 types: (pathologically) Subendocardial infarction Transmural infarction (clinically) Non-STEMI STEMI


can occur in various regions of the heart wall and may be described as anterior, inferior, posterior, lateral, subendocardial, or transmural, depending on the location and extent of tissue damage from infarction.


infarcted myocardium is surrounded by a zone of hypoxic injury, which may progress to necrosis or return to normal, adjacent to this zone of hypoxic injury is a zone of reversible ischemia

Wall of the Heart: Pericardium -the double-walled membranous sac that encloses the heart Myocardium -composed of cardiac muscle and is anchored to the hearts fibrous skeleton Endocardium -connective tissue and a layer of squamous cells found in the internal lining of the myocardium

-when coronary blood flow is interrupted for an extended period, myocyte necrosis occurs. This results in MI. -in the majority cases of MI, the decrease in coronary flow is the result of atherosclerotic CAD -other causes include coronary spasm and coronary artery embolism

- most common cause of death in the UK -approximately 300,00 new MI per year -only half of those who suffer an MI survive the acute event -further 10% die in hospital and up to 10% more die in the following 2 years -50% of initial survivors are alive at 10 years

-plaque progression -disruption

-subsequent clot formation

-thrombus is less labile and occludes the vessel for a prolonged period, such that myocardial ischemia progresses to myocyte necrosis and death -Subendocardial infarction

if thrombus breaks up before complete distal tissue necrosis has occurred, the infarction will involve only the myocardium directly beneath the endocardium
this infacrtion presents with ST depression and T wave inversion without Q waves, so it is termed non-STEMI. important to recognize his form of acute coronary syndrome because recurrent clot formation on the disrupted atherosclerotic plaque is likely unless some intervention is undertaken as soon as possible if the thrombus lodges permanently in the vessel, the infarction will extend through the myocardium all the way from endocardium to epicardium, resulting in severe cardiac dysfunction individuals who have this kind of infarction usually have marked elevations in the ST segment on ECG and are categorized as having STEMI important to identify those individuals with transmural infarction who are at highest risk for serious complications and who should receive definitive intervention without delay

-Transmural infacrtion

- with an acute myocardial infarction, blood pressure may initially decrease. The drop in blood pressure reflexively activates the sympathetic nervous system to compensate and increase the HR in an effort to restore the blood pressure. Blood pressure may remain low (hypotension) or may become elevated depending on the severity of myocardial damage.

-the first symptom is sudden, severe, and prolonged chest pain -pain may be described as heavy and crushing, such as a truck sitting on my chest -radiation to the neck, jaw, back, shoulder, or left arm is commonsome individuals (especially older adults or those with diabetes) experience no pain, thereby having a silent infarction -infarction often stimulates a sensation of unrelenting indigestion -nausea and vomiting may occur because reflex stimulation of vomiting centers by pain fibers -vasovagal reflexes from the area of the infarcted myocardium also may affect the gastrointestinal tract -catecholamine release results in sympathetic stimulation, producing diaphoresis and peripheral vasoconstriction that cause the skin to become cool and clammy -cardio vascular changes

dysrhythmias (arrhythmias) - most common complication of acute myocardial infarction, affecting more than 90% of individuals pericarditis (inflammation of the pericardium) -pericardial friction rubs often are noted 2-3 days after MI and are associated with anterior chest pain that worsens with respiratory effort dressler postinfarction syndrome (delayed form of acute MI) -occur from 1 week to several months after acute MI -thought to be immunologic (antigen-antibody) response to the necrotic myocardium -pain, fever, friction rub, pleural effusion, and arthralgias may accompany this syndrome organic brain syndrome -may occur in acute or chronic form if blood flow to the brain is impaired secondary to MI cardiac complication -rupture of heart structures: 1. necrosis of tissue in or around the papillary muscles can cause rupture of these muscles or chordate tendinae 2. infarction around septal structures that separate the heart chambers can lead to septal rupture

Cardiac Rehabilitation MI Tissue changes after myocardial infarction

Phase Phase

I: Inpatient component II: Out patient

Exercise Training Period


III: Maintenance

When to start aerobic & strength training? After the ETT result When can ETT be given after MI? After MI, wound healing begins; wound is stable within in 4 to 6 weeks ETT is within 4 to 6 weeks

Hospital stay is 3-5 days Components: selected arm & leg exercise, supervised ambulation, ADLs Role of PT: Monitor activity tolerance Educate the patient to recognize adverse symptoms with activity Support risk factor modification techniques Provide emotional support Collaborate with other team member Goal: 20-30 minutes of ambulation 1-2 min/day at 4-6 weeks post MI VS monitoring: before, after, if possible during activity Intensity: Low intensity: start at 2-3Mets-> 3-5 at discharge Borgs RPE: fairly light range HR increase of 10-20 bpm(depending on meds) Increase 1 to 2 METs = HR increase by 10 to 20 bpm uncommon if with beta blocker

Important concepts prior to discharge: Symptom Recognition Appropriate activity guidelines- consider environmental conditions Question: Can I buy equipment I saw on TV so I can continue my exercise at home? Patients should be monitored on similar equipment for safety before doing the exercise at home This is NOT the time to for a patient to try a new type of exercise modality Walking is exercise of choice ease and familiarity

Rationale of Treatment: Improve functional capacity Progress toward full resumption of ADL, habitual & occupational activities Promote risk factor modification, counseling as to lifestyle changes Encourage activity pacing, energy conservation; stress importance of taking proper rest period Patient commonly undergo a symptom-limited maximal stress test (ETT) at 4-6 weeks post MI If without ETT: Use 70-80% or 65-80% of HRmax If with ETT: MVO2 below the patient ischemic threshold Clinical measure of MVO2 is RPP(rate pressure product) RPP = HR x Systolic BP Do NOT exceed 90% of patients RPP


program: average 36 visit (3/wk x

12wk) Frequency: 3-4 sessions/week Intensity: 5 METs (needed for most ADL) to 9 METs Time: 30-60 min w/ 5-10 min of warm-up & cool down Type: single mode or multiple modes, circuit training


of Treatment: Improve and/or maintain functional outcome Promote self-regulation of exercise programs Promote life long commitment to risk-factor modification Discharge in 6-12 months Location: community center, PRT gym, or clinical facilities Progression: supervised -> self-regulation


Kathryn I. and et al. Pathophysiology the biologic basis for disease in adults and children. 5th Ed. Missouri: Mobsy Elsevier, 2010. p.1171 & Clark. Pathophysiology. 5th Ed. WB Saunders, 2002. p.774 medsurge under Doc Arco