CARDIOVASCULAR PHYSICAL THERAPY

A. The Heart and Circulation

1. Heart tissue
pericardium ( parietal, visceral) epicardium myocardium endocardium

2. Heart chambers
(R) atrium/ ventricles, (L) atrium/ ventricles

CHAMBERS
ATRUIM
thin walled with fair amount of elasticity and distensibility low pressure chamber

VENTRICLES
Thick walled High pressure

chamber

3. Valves
AV valves

tricuspid / bicuspid (mitral) attached by chordae tendinae that prevents valvular prolapse during ventricular systole Semilunar valves pulmonary / aortic open during ventricular systole & close during diastole

Atrioventricular valve (AV valve) prevent backflow of

blood from the ventricle to the atria. a) tricuspid valve b) mitral valve (bicuspid)

mitral

tricuspid
pulmonic aortic

Semilunar valves ( SL valve )

thicker than the

AV valve prevent backflow of blood from the aorta or pulmonary to the ventricles a) pulmonary b) aortic valve

HEART SOUNDS
A) First heart sound low pitched lub sound, due to closure of the AVvalves. B) Second heart sound high-pitched dub sound, due to closure of the SL valves. C) Third heart sound due to rapid ventricular filling. May indicate CHF in older individual D) Fourth heart sound due to atrial systole. May indicate CAD, MI, aortic stenosis

4. Coronary circulation

Coronary Arteries: arise directly from aorta near aortic valve; blood circulates to myocardium during diastole. RCA
RA most of RV inferior wall of the LV SA node (60%) AV node bundle of His

LCA
LAD LV, RV (some) Circumflex artery: lat & inf. wall of LV portion of LA SA node (40%)

Coronary Sinus - receives venous blood from the heart and empties into the RA

SINOATRIAL NODE OR SA NODE

(Node of Keith and Flack) Pacemaker of heart Initiates an electrical impulse at a rate higher than any other part of the myocardium

ATRIOVENTRICULAR NODE OR AV NODE (Node of Kent and Tawara)

theres a delay in impulse conduction from the atria to the ventricle ( AV nodal delay ) slowest velocity of conduction small size of the fiber RMP is much less negative

BUNDLE OF HIS
begins at the AV node and penetrate the upper portion of the interventricular septum Right bundle branch Left anterior bundle posterior bundle Transmits and distributes signal rapidly through ventricles

PURKINJE FIBERS velocity of conduction is fastest

ELECTROCARDIOGRAM

What is Electrocardiogram?
ECG or EKG is the record of the electrical activity of the heart during cardiac cycle. this record represents the algebraic sum of the action potentials of myocardial fibers

SAN depolarization
The events of the cardiac cycle are initiated by depolarization of the sinoatrial node

Atrial depolarization
The wave of electrical depolarization is conducted through the cardiac muscle of both atria

Atrial contraction
The depolarizing wave causes contraction of the atria pushing blood into the ventricles

AV Node depolarization
The wave of depolarization reaches the fibrous septum, which does not conduct the atrio-venticular node which depolarizes and conducts, but slows the wave

Bundle Of His
The AVN conducts the depolarization to the Bundle of His The Bundle of His continues as the the Right and Left Bundle Branches These tissues rapidly conduct the impulse

Ventricular depolarization
The wave of depolarization quickly moves through the specialised conducting tissue Ventricular muscle is depolarized in a coordinated, synchronised manner

Ventricular contraction
The coordinated, synchronised depolarization produces an effective contraction of both ventricles Blood is pushed into the aorta and pulmonary veins (not shown)

Ventricular repolarization
After depolarization and contraction the ventricle repolarise Repolarization returns the ventricles back to their resting potential

SAN depolarization
SAN depolarization initiates atrial depolarization occurring at the end of iso-electrical line

Atrial depolarization
The P wave represents atrial depolarization

AVN depolarization
AVN depolarization occurs within and is responsible for most of the PR interval

Ventricular depolarization
The depolarization of the special conducting tissue and ventricles causes the QRS complex

Ventricular repolarization
Repolarization of the ventricles produces the T wave

Relationship of electrical events to ECG

SA node Atrial depolarisation (P wave) AV node (main component of PR interval) Bundles of his and ventricular depolarisation (QRS) Ventricular repolarisation (T waves)

Cardiac Diseases

Coronary Artery Disease

Coronary Artery Disease

An atherosclerotic disease process that narrows the lumen of coronary arteries, resulting in ischemia to the myocardium.

The impairment is an imbalance of myocardial oxygen supply to meet the myocardial oxygen demand.

What is Atherosclerosis?
Characterized by thickening of

the intimal layer of the blood vessel wall from focal accumulation of lipids, platelets, monocytes, plaque and other debris. Smooth muscle cells proliferate & fatty substance accumulation in the wall

It is an inflammatory reaction in
response to injury

Non-modifiable Risk factors

age sex race family history of CAD

Modifiable Risk Factors

1.Cigarette smoking

2.High BP
3.Obesity

4.Increase cholesterol and LDL levels

5.Inactivity

6.Stress
7.DM

Main Clinical Syndromes of CAD

Angina Pectoris Myocardial Infaction Heart Failure Sudden Death

1. Angina pectoris substernal chest pain or pressure may be accompanied by Levines sign
the holding of a clenched fist over chest to describe constricting, pressing pain typical of angina pectoris

1. Angina pectoris represents imbalance in myocardial oxygen supply and demand brought on by:
a. demands on heart by: exertion, emotional stress, smoking, extremes of temperature (cold), tachyarrhythmias b. vasospasm Prinzmetals angina

Types:
a. Stable angina classic exertional angina it occurs at predictable rate-pressure product (RPP) = HR x BP (systolic) relieved with rest and/or nitroglycerin

b. Unstable angina A.k.a. preinfarction, crescendo angina coronary insufficiency with risk for MI or sudden death typically occurs at rest pain is difficult to control doesnt occur at predictable RPP

Anginal Scale
1+ 2+ 3+ 4+ light, barely noticeable moderate, bothersome severe, very uncomfortable most severe pain ever experienced

2. Myocardial Infarction (MI)

result from prolonged ischemia, injury and death of an area of myocardium caused by occlusion of one or more coronary arteries. irreversible changes in most myocardial cells when ischemia lasts from 20 minutes to 2 hours.

Precipitating factors: 1. Atherosclerotic heart disease with thrombus formation 2. coronary vasospasm or embolism 3. cocaine toxicity

Zones of Infarction
1. Central zone / Zone of infarction consist of necrotic, noncontractile tissue on EKG, pathological Q waves 2. Zone of injury consist of noncontractile tissue cells undergoing metabolic changes electrically unstable on EKG, elevated ST segment

3. Zone of ischemia the outer area cells undergoing metabolic changes electrically unstable on EKG, T wave inversion

Infarction sites

1. Transmural full thickness of the myocardium Q wave infarctions 2. Nontransmural subendocardial, subepicardial, intramural infarction non Q wave infarctions

Sites of Coronary artery occlusion

1. Inferior MI
right ventricle infarction disturbances of upper conducting system involves RCA

2. Lateral MI
ventricular ectopy, involving circumflex artery

3. Anterior MI
disturbances of lower conduction system involving LAD artery

Impaired ventricular function results in:

1. SV, CO & ejection fraction 2. end diastolic ventricular pressures 3. Electrical instability arrhythmias, present in injured and ischemic areas

Major complications:
Ongoing ischemia LV failure Ventricular arrhythmias

Ultimate complication:
Cardiogenic Shock inadequate CO and arterial BP to perfuse the major organs as a result of severe LV failure * Wound is established within the first 4-6 wks

What is a Heart Failure ?

Cardiac failure CHF A condition in which the heart is unable to maintain adequate circulation of the blood to meet the metabolic needs of the body.

Etiology:
CAD Valvular diseases CHD Hypertension Infections

Physiological abnormalities:

CO end diastolic pressures (preload) HR Impaired ventricular function Cardiomyopathy (hypertrophy)

Types:
A. Left heart failure
a.k.a. Forward heart failure blood is not adequately pumped into systemic circulation due to an inability of left ventricle to pump

pulmonary artery pressures & Pulmonary Edema

Signs & symptoms:

Fatigue Cough SOB (shortness of breath) DOE (dyspnea on exertion) Orthopnea PND (paroxysmal nocturnal
dyspnea)

Diaphoresis Weakness

Tachycardia Crackles Pulsus alterans Confusion Decreased urine output Murmur of mitral insuff. Cheyne-Stokes resp.

B. Right heart failure

a.k.a. Backward heart failure blood is not adequately returned from the systemic circulation to the heart due to failure of the RV & Pulmonary hypertension CO renal failure

Signs & symptoms:

Nausea Anorexia Weight gain Ascites UQ pain Increased AP, CVP Jugular vein distention Murmur of tricuspid insuff. Hepatomegaly Peripheral edema

What is Arrhythmia?
Abnormal, disordered rhythm Caused the heart to beat too fast, too slow or irregularly Etiology:
MI Electrolyte imbalance Acidosis or alkalosis Hypoxemia Hypotension Emotional stress Drugs, alcohol, caffeine

Types:
1. Tachycardia 2. Bradycardia

Sinus tachycardia
A sinus rhythm of higher than 100/min is called sinus tachycardia. Impulses originate at S-A node at rapid rate It occurs most often as a physiological response to physical exercise or psychical stress, but may also result from congestive heart failure.

Sinus bradycardia
A sinus rhythm of less than 60/min is called sinus bradycardia. Impuses originate at S-A node at slow rate This may be a consequence of increased vagal or parasympathetic tone.

Atrial Tachycardias
Rapid and repetitive firing of one or more ectopic foci in the atria a. Premature Atrial Contractions (PACs) b. Paroxysmal Supraventricular tachycardia (PSVT) c. Atrial flutter d. Atrial fibrillation
e. Wolff-Parkinson-White Syndrome

Premature Atrial Contractions

Ectopic beat originates in the atria and may present as irregular rhythm Will not compromise the CO

Paroxysmal supraventricular tachycardia (PSVT)

a.k.a. paroxysmal atrial tachycardia (PAT). These arrhythmias are common in young people Common cause is digoxin toxicity HR : 140 250 bpm

Atrial fibrillation (A-fib)

Classic irregular rhythm a rapid, irregular heartbeat HR: >300 bpm is seldom a life-threatening arrhythmia, but over time it can be the cause of more serious conditions such as stroke. Avoid PT intervention if the patients HR is greater than 115 bpm
,

Atrial flutter
Similar to atrial fibrillation,

both can coexist beats regularly, although at a much faster pace than normal HR: 250 350 bpm Tx: Defibrillation and Beta Blockers

5. Wolff-Parkinson-White Syndrome
caused by an extra electrical pathway between the atria and the ventricles. This pathway may allow electrical current to pass between the atria and the ventricles without passing through the AV node, leading to short circuits and rapid heartbeats can cause other types of tachycardia, including atrial flutter and atrial fibrillation Tx: beta blockers and calcium channel blockers

Wolff-Parkinson-White syndrome

Tachycardias in the Ventricles

Adversely affects the cardiac output Types: a. Premature ventricular contractions (PVCs) b. Ventricular tachycardia c. Ventricular fibrillation

Premature Ventricular Contractions

A premature beat arising from the ventricle Occurs occasionally in the majority of the normal population On ECG: no P wave; bizarre & wide QRS Serious: > 6 per minute

Ventricular tachycardia
A run of 3 or more PVCs occurring

sequentially fast, regular beating of the heart is caused by abnormal electrical impulses originating in the ventricles Very rapid rate (150-200 bpm)
HR
CO

 On ECG: wide bizarre QRS; no P wave Medical intervention should be initiated ASAP No PT intervention Initiate CPR Activating ACLS

Ventricular fibrillation
rapid, chaotic electrical impulses that cause ventricles to quiver uselessly instead of pumping blood VF can originate from many different locations in the ventricles Ventricles do not contract No effective CO Clinical death within 4-6 min.

 On ECG: bizarre, erratic act. QRS complex Activate ACLS with electrical defibrillation & medications

Electrical Defibrillation

Bradycardias
1. Sinus bradycardia sinus node isn't sending impulses properly Causes: hypothyroidism drug side effect Treatment: pacemaker

2. Atrioventricular blocks Abnormal delays or failure to conduct through normal conducting system a. First degree b. Second degree c. Third degree Life threatening Requires medication (atropine) Surgical implantation of pacemaker

First-degree atrioventricular block

the P-wave always precedes the QRS-complex but the PR-interval is prolonged over 0.2 s Atrio-ventricular conduction lengthened

Second-degree atrioventricular block

the PQ-interval is longer than normal and the QRScomplex sometimes does not follow the P-wave If the PR-interval progressively lengthens, leading to the dropout of a QRS-complex, the second degree block is called a Wenkebach phenomenon.

Third-degree atrioventricular block

Complete lack of synchronism between the P-wave and the QRS-complex Impulses originate at AV node and proceed to ventricles Atrial and ventricular activities are not synchronous

What is Stokes-Adams Syndrome?

Dizziness and fainting caused by cerebral ischemia resulting from a decrease in CO

What is Brugada syndrome?

is an abnormality in the heart's electrical system that causes life-threatening arrhythmias. occurs most often in young adults. It also occurs with increased frequency in Asians.

What is Pericarditis ?
Is an inflammation of the epicardium and parietal pericardium may result into accumulation of fluid in the pericardial sac, preventing the heart from expanding & reduces CO

Signs & Symptoms

Substernal pain Relieve by leaning forward or by sitting upright Aggravated by movement and asso. with deep breathing(laughing, coughing, deep inspiration) Difficulty in swallowing History of fever, chills, weakness or heart disease

What is Cardiac Tamponade?

Is a life-threatening complication caused by accumulation of fluid in the pericardium this fluid accumulates fast enough and in sufficient quantity to compress the heart and restricts blood flow in and out of the ventricles
This is a cardiac emergency!

What is Aneurysm?
Is an abnormal dilatation in the weakened and diseased arterial wall Causes:
trauma congenital vascular disease infection atherosclerosis

Sites:
Thoracic aneurysm

ascending, transverse or descending aorta

Abdominal Aortic Aneurysm (AAA)

aorta between renal arteries & iliac branches

Peripheral arterial aneurysm

femoral & popliteal arteries

Valvular Diseases
Caused by : 1. Disease (Rheumatic fever or coronary thrombosis) 2. Congenital deformity 3. Infection (Endocarditis)

Types
1. Stenosis
narrowing or constriction that prevents the valve from opening fully may be caused by growths, scars or abnormal deposits on the leaflets Aortic Stenosis

2. Insufficientcy (Regurgitation)
occurs when the valve does not close properly and causes blood to flow back into the heart chamber

3. Prolapse
affects only the mitral valve and occurs when enlarge valve leaflets bulge backward into the atrium

Signs & symptoms

Easy fatigue Dyspnea Palpitation Chest pain Pitting edema Orthopnea or paroxysmal dyspnea Dizziness or syncope

What is Rheumatic Fever?

Is an infection caused by streptococcal bacteria that can be fatal or may lead to rheumatic heart disease. most common symptoms: fever & joint pain most commonly affects : mitral & aortic valves

Signs and symptoms:

Arthritis Fever Carditis Subcutaneous nodules Erythema marginatum Chorea Abdominal pain

What is Rheumatic chorea?

a.k.a. St. Vitus dance may occur 1 - 3 months after strep. infection and always occur after polyarthritis rapid, purposeless nonrepetitive movements that may involve all muscles except the eyes may last for 1 wk or several months

What is Rheumatic Heart Disease?

Mitral valve prolapse secondary to rheumatic fever may be asymptomatic or may present with symptoms that are poorly related to exertion and do not subside with rest or nitroglycerin mitral regurgitation is present

Signs & symptoms

Nonanginal chest pain Palpitations Fatigue Dyspnea

What is Endocarditis?
Inflammation of the cardiac endothelium caused by infection damages the tricuspid, aortic or mitral valve (vegetations) May be caused by bacteria or may occur as a result of abnormal growths(consist of collagen fibers) on the closure lines of previously damaged valves often a consequence of receiving dental treatment

Signs & symptoms:

Fever Night sweats Petechiae of the skin & mucus of eyes & mouth splinter hemorrhages in the nail beds recurrent influenza-like illness headaches musculoskeletal complications: myalgias, arthralgias, back pains

Cardiomyopathy
Is a heart muscle disorder of unknown cause Types: Dilated, Hypertrophic, Restrictive Risk factors: alcoholism pregnancy systemic hypertension various infections

Three main types of nonischemic cardiomyopathies:

1. Dilated cardiomyopathy (including peripartum cardiomyopathy and alcoholic cardiomyopathy) involves dilation or enlargement of the hearts ventricles and is usually accompanied by an increase in cardiac mass This often affects young people.

2. Hypertrophic cardiomyopathy involves an abnormal growth of muscle fibers in the heart muscle, usually in the left ventricle. This is usually considered a genetic disorder. Severe thickening of the heart muscle may cause obstruction of blood flow from the left ventricle to the aorta, resulting in low heart output, fatigue, fainting and arrhythmias

3. Restrictive cardiomyopathy which means the heart muscle cannot adequately relax after contraction, making it unable to fill completely with blood. This condition is distinguished from some forms of hypertrophic cardiomyopathy because the left ventricle is frequently normal sized.

Medical Management of Cardiovascular Disease

1. 2. 3. 4.

Diet Medications Activity restrictions Surgical interventions

Diet
low salt high in fiber

 low cholesterol

 weight reduction

Pharmacological Therapy

Nitrates
e.g. nitroglycerin decrease preload through peripheral vasodilation reduce myocardial O2 demand reduce chest discomfort (angina) improve coronary blood flow

Beta adrenergic blocking agents

e.g. propanolol (inderal)
metoprolol (Lopressor) inhibit the effect of sympathetic nervous system reduce myocardial O2 demand by HR & cardiac contractility control arrhythmias, chest pain BP

Calcium channel blocking agents

e.g. amlodipine (norvasc), ditiazem (cardizem), nifedipine (Procardia), verapamil (Isoptin, Verelan) inhibit flow of calcium ions HR, and cardiac contractility dilate coronary arteries BP control arrhythmias and chest pain

ACE (angiotensin-converting-enzyme) inhibitors

e.g. Captopril (Capoten)
benazepril (Lotensin) enalapril (Vasotec) suppress the renin-angiotensin-aldosterone system, blocking the production of the potent vasoconstrictor angiotensin II result in renal blood flow which enhances diuresis Control high blood pressure Treat CHF

Antiarrhythmics
e.g. Quinidine, Procainamide, lidocaine (xylocaine) alter conductivity restore normal heart rhythm control arrhythmias improve CO

Antihypertensives
e.g. Propanolol Reserpine control hypertension the goal is to maintain diastolic pressure less than 90 mmHg decrease afterload myocardial O2 demand

Digitalis (cardiac glycosides)

e.g. Digoxin (Lanoxin)

increase ventricular contractility

(+ inotropic effect) augments SV HR & CO (therapeutic response) mainstay in the treatment of CHF SIDE EFFECTS: weakness & palpitations

Diuretics (water pills)

e.g. Furosemide (Lasix), Hydrochlorothiazide (Esidrix) enhance renal excretion of sodium and water blood volume, preload & afterload decrease myocardial work control hypertension

Inotropic agents
Dopamine, Dobutamine, Amninone

for patient with low output HF facilitate myocardial contractility SV CO renal blood flow & GFR

Anticoagulants or Blood thinners

Warfarin (Coumadin - oral)

Heparin (Calciparin - IV) decrease platelet aggregation may prevent MI

Platelet Inhibitors
Acetylsalicilic acid (aspirin) Dipyridamole (Persantine) Plavix

Prevent recurrent clot formation

Prevent the sudden re-closing of a coronary artery (after PTCA)
(percutaneous transluminal coronary angioplasty)

Prevent stroke and heart attack

Hypolipidemic agents
e.g. Atorvastatin (lipitor), simvastatin (Zocor), lovastatin (Mevacor) cholestyramine(Questran), colestipol (Colestid)
reduce serum lipid levels when diet and weight reduction are not effective They lower cholesterol by as much as 45-50% raise HDL while lowering LDL and triglyceride

Tranquilizers
Benzodiazepines Ativan (lorazepam), Rivotril (clorazepam), Valium (diazepam). Sleeping pills : Imovane (zopiclone)

decrease anxiety, sympathetic effect

central nervous system depressants

3. Activity restriction
acute MI, CHF limited generally to 1st 24 hours or until the patient is stable for 24 hours

Surgical Interventions

What is an Angiogram?

An angiogram is an invasive procedure done to find the blockages in the coronary arteries.

What is Angioplasty?

Percutaneous Transluminal Coronary Angioplasty under fluoroscopy, surgical dilation of a blood vessel using a small balloon-tipped catheter inflated inside the lumen result in improve coronary BF, improved LV function and anginal relief

Intravascular stents
an endoprosthesis (pliable wire mesh) implanted postangioplasty to prevent restenosis and occlusion in coronary or peripheral arteries

Revascularization surgery (CABG)

What is Coronary Artery Bypass Surgery?

is an open-heart surgery that is done to reroute or "bypass" blood around blocked arteries. uses an anastomosing graft saphenous vein internal mammary artery radial artery result in improved coronary blood flow

What is Cardiac Rehabilitation?

A multidisciplinary team promotes behaviors to help you and your family adapt to a new life style The program is directed toward restoring and maintaining optimal physiological, psychological, vocational, and social well-being while reducing the risk of future heart problems.

Normal Response:
1. Cardiac output and heart rate will increase in a linear relationship with the increase in work load and oxygen consumption demand 2. Maximum HR will decrease with age 220 - age 3. BP : systolic will rise but diastolic will remain level or slightly increase

Abnormal response:
1. On EKG: ST segment depress/elevate 2. BP Systolic : will remain level during exercise or remain high after exercise Diastolic: will above 20 mmHg or after exercise 3. Angina symptom during exercise 4. Abnormal HR STOP exercising if any of the above occur during exercise

Possible Benefits of a Cardiac Rehabilitation Program

1. Decrease HR at rest & during exercise; improve HR recovery after exercise 2. Increased SV 3. Increased myocardial oxygen supply and myocardial contractility 4. Improved respiratory capacity during exercise 5. Improve functional capacity of ex. muscle

7. Reduced body fat, increase lean body mass 8. Decreased serum lipoproteins 9. Improve glucose tolerance 10. Improve blood fibrinolytic activity & coagulability 11. Improvement in measures of psych. Status 12. Increased participation in exercise

Unstable angina Fever Thrombophlebitis Uncontrolled diabetes Acute illness Uncontrolled dysrhythmias Uncontrolled tachycardia Recent embolism Third-degree heart block Symptomatic CHF Resting systolic BP over 200 mmHg Resting diastolic BP over 100 mmHg

Guidelines for Exercise Prescription

Type Intensity Duration Frequency

A. Type
1. Cardiorespiratory endurance activities
recommended to improve exercise tolerance walking, jogging, or cycling

2. Dynamic arm ex. (arm ergometry)

uses a smaller muscle mass, result in lower VO2 max (60-70% lower) than leg ergometry at a given workload, HR will be higher SV lower systolic/diastolic BPs will be higher

3.Other aerobic activities

swimming, cross country skiing less frequently used due to high inter-individual variability energy expenditure related to skill level

4. Warm-up and cool-down activities gradually increase or decrease the intensity of exercise to promote circulatory and muscular adjustment to exercise low intensity cardiorespiratory endurance activities, flexibility ex., functional mobility activities

5. Resistive exercises improve strength and endurance in clinically stable pts. prescribed after a period of aerobic conditioning moderate intensities are typically used monitor BP, avoid Valsalva response CI : poor LV function, ischemic changes on EKG during ETT, functional capacity less than 6 METS, uncontrolled hypertension or arrhythmias

6. Relaxation training
relieves generalized muscle tension and anxiety usually incorporated after an aerobic training session and cool-down assist in successful stress management and life-style modification

B. Intensity
prescribed as percentage of functional capacity revealed on ETT, within a range of 40-85% depending upon the initial level of fitness typical training intensity is 60-70% of functional capacity

1. Heart rate a. Maximum HR HR max = 220 - age (UE, = 220 - age -11) 70 - 85% HR max, it closely correspond to 60-80% of functional capacity or VO2 max
used in cases where submaximal ETT has been given

b. Heart rate range

Karvonen formula Target HR = 60-80% (HRmax - resting HR) + resting HR more closely approximates the relationship between HR and VO2max

Should not be used on individuals taking beta blocking or calcium channel blocking medications.

2. Rating of perceived exertion (RPE)

somewhat hard (12-13 original Borg scale) or somewhat strong (4 Borg 10-grade scale) correspond to 60% of HR range RPE of hard or strong correspond to 85% of HR range may find problem if use in individual with psychological condition (depression)

3. METs or estimated energy expenditure (VO2)

Problems : varying skill level or stress of competition may affect the known metabolic cost of an activity

environmental stresses (Heat, cold, high humidity, altitude, wind, change in terrain) may affect the known metabolic cost

C. Duration
Conditioning phase : 15 - 60 min. depending upon the intensity ( higher I, shorter D) Average conditioning time: 20-30 min (for moderate intensity exercise) Severely compromised : 3 min-sessions warm-up & cool-down : 5 - 10 min.

D. Frequency
depending upon the intensity and duration the lower the intensity, the shorter the duration, the greater frequency Average : 3 - 5 sessions/week for ex. at moderate intensities and duration (>5 METS) Daily or multiple daily sessions for low intensity exercise (< 5 METS)

Progression
modify exercise prescription if: HR is lower than THR for a given ex. intensity RPE is lower symptoms of ischemia do not appear rate depends on age, health status, functional capacity, personal goals, preferences. Duration is increased first, then the intensity

Consider reduction in exercise/activity with:

acute illness (fever, flu) acute injury progression of cardiac disease: edema, unstable angina overindulgence: food, caffeine, alcohol drugs : decongestants, bronchodilators, atropine environmental stressors: extremes of heat, cold, humidity; air pollution

GOALS:
Initiate early return to independent ADL Counteract deleterious effects of bed rest Help allay anxiety and depression Provide medical survaillance Provide patient and family education Promote risk factor modification

Exercise Guidelines
Type of Ex: ADLs, selected arm and leg ex., early supervised ambulation Low intensity: 2-3METs 3-5 METs RPE: Fairly light HR increase of 10-20 above resting Short exercise sessions, 2-3x/day

GOALS:
Improve functional capacity Progress toward full resumption of ADL, habitual and occupational activities Promote risk factor modification, counseling as to life-style changes Encourage activity pacing, energy conservation, importance of taking proper rest periods.

Exercise Guidelines
Average of 36 visits allowed Type of ex.: single mode training or circuit training strength training Duration: 30 60 min; 5-10 min warm-up/cool-down Frequency : 3-4 sessions/week Suggested exit point: 9 METs

Guidelines for Strength training

After 3 weeks cardiac rehab; 5 wks post MI; 8 weeks post CABG Begin with use of elastic bands & light wts. (1-3 lbs.) Progress to moderate loads; 12-15 repetitions

ULTIMATE GOAL: HEALTHY LIVING

GOALS:
Improve and/or maintain functional capacity Promote self-regulation of exercise programs Promote life-long commitment to risk-factor modification

Exercise Guidelines
Location: Community centers, YMCA or clinical facilities Entry level : 5 METs; clinically stable angina; medically controlled arrhythmias during exercise Progression: supervised self-regulated exercise Progress to 50-85% of functional capacity 3-4x/week, 45 min or more/ session d/c in 6-12 months.