Cardiac Rehab

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
 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 Arteries: arise directly from aorta near
aortic valve; blood circulates to
myocardium during diastole.

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)
 there’s 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 intervevtricular
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)
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.
• Characterized by thickening of
the intimal layer of the blood
vessel wall from focal
accumulation of lipids, platelets,
monocytes, plaque and other
debris.
What is Atherosclerosis?
• 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
 Angina Pectoris
 Myocardial Infaction
 Heart Failure
 Sudden Death
Main Clinical
Syndromes of CAD
1. Angina pectoris
 substernal chest pain or pressure
 may be accompanied by Levine sign
 represents imbalance in myocaldial oxygen
supply and demand brought on by:
a. demands on heart by: exertion, emotional
stress, smoking, extremes of temperature (cold),
tachyarrhythmias
b. vasospasm – Prinzmetal’s 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,
cresendo angina
 coronary insufficiency with
risk for MI or sudden death
 typically occurs at rest
 pain is difficult to control
 doesn’t occur at predictable
RPP

Anginal Scale
1+ light, barely noticeable
2+ moderate, bothersome
3+ severe, very uncomfortable
4+ 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
• DOE
• Orthopnea
• PND
• Diaporesis
• Weakness
• Tachycardia
• Crackles
• Pulsus alterans
• Confussion
• Decrease 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
 RUQ pain
 Increased RAP, CVP
 Jugular vein distention
 Murmur of tricuspid insuff.
 Hepatomegally
 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.
 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
Atrial Tachycardias
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 patient’s 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 QRS-
complex 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
restriction 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 heart’s
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. Diet
2. Medications
3. Activity restrictions
4. 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 O
2
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 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 O
2
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)
 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?
 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
Percutaneous Transluminal Coronary
Angioplasty
Intravascular stents
 an endoprosthesis
(pliable wire mesh)
implanted post-
angioplasty 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

 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
2. Dynamic arm ex.
(arm ergometry)
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 VO
2
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 VO
2
max
 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 (VO
2
)
 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.