Download Cardiopulmonary Study guide #1 Lecture #1 anatomy of the heart 1

Cardiopulmonary Study guide #1
Lecture #1 anatomy of the heart 1/8/15

Know anatomy of heart

Cardiac circulation
o R atria—tricuspid valve—R ventricle—pulmonary valve—lungs—L atria—mitral valve—L
ventricle—aortic valve—aorta—body

Coronary Vasculature
o Right coronary artery

R marginal artery

R posterior descending
o L coronary artery

L circumflex

L anterior descending
o Great cardiac veins
o Coronary sinus
o R coronary Artery

R atria

Posterior R ventricle

SA and AV nodes

Bundle of HIS
o R marginal artery

Posterior R ventricle

Diaphragmatic margin of both ventricles
o R posterior descending

Posterior interventricular septum

inferior L ventricle
o L anterior descending Artery

Anterior L ventricle

Anterior interventricular septum and adjacent R ventricle

Portions of bundle branches

Proximal/inferior portions of ventricles and apex
o L circumflex

Superior and marginal L ventricle

Posterior L ventricle

L atrium
o Cardiac Veins

Coronary sinus

Left marginal and posterior interventricular

Middle and small cardiac veins

Anterior cardiac veins

Peripheral circulation
o Head and neck

Carotid arteries

Temporal arteries
o Upper extremity

Brachial arteries

Radial arteries
o Abdominal aorta
o Lower extremity

Femoral A

Popliteal a

Posterior tibial

Dorsalis pedis

Cardiovascular responses to exercises
o Cardiac output-amount of blood ejected per minute
o Stroke volume- blood ejected per beat
o Systole- heart is contracting
o Diastole- heart is relaxed, fills with blood
o Total peripheral resistance-resistance to BF
o Blood pressure- CO times TPR BP= CO x TPR
o VO2- a measure of the body’s capacity to oxygenate
o A-v O2 difference- O2 difference from arterial to venous represents uptake
o

Ve=minute ventilation-amount of air moved into or out of the lungs per unit time; equals the
product of the tidal volume (Vt) and the respiratory rate
Response to a single bout of exercise
o Cardiac adaptations

The CV system responds in the greatest magnitude

Redistribution of blood to areas with an increase in metabolic demand

Lowering of blood flow to non-essential organs during exercise

Heart rate

The increase in HR is proportional to intensity of activity

Linear relationship between HR and oxygen consumption

Stroke volume- increase in force of contraction leading to increase SV

Factors that influence SV:
o Preload

Amount of tension on the muscle before it contracts

Volume of blood in the ventricles after filling (end-diastolic
volume)

Ventricular filling pressure

Positive effect on CO (stroke volume)- high preload, SV
high; low preload, SV low
o Contractility

Muscular performance of the heart

Rate and intensity of force development during contraction

Positive effect on CO
o Afterload

Pressure against which the ventricle must work to eject
blood (resistance to flow from the heart)

Negative effect on CO

Afterload is reflected in diastolic BP

High DBP means high resistance to overcome
o Exercise intensity

HR and SV increases at 40-60% of maximum capacity

At higher intensities, CO increases by HR elevation, not by
SV
o Coronary circulation adjustments

Closely linked to metabolic needs of the heart muscle

Heart muscle cells are highly oxidative

Coronary circulation occurs during diastole

During rest muscle extracts approximately 70% of oxygen delivered

During exercise-demands are met by:

Increasing rate of BF

Increasing the aortic pressure
o Systemic circulation adjustments

Blood is shunted from less active tissues

Increase in BF to the lungs

Increase BF to active muscles leading to O2 delivery and better oxygen extraction

To dissipate heat, BF to skin increase

SEE PIC ON PAGE 5
o BP adjustments

BP= CO x TPR

Blood vessels dilate leading to decrease in resistance

Negated by increase in CO

Net effect is systolic pressure increases

Increase is proportional to intensity and O2 demand of activity

Factors affecting arterial BP

Physiological factors
o CO
o TPR

Physical factors
o Arterial BV
o Arterial compliance
o Respiratory adjustments




Minute ventilation increases Ve=RF xTV
Linear relationship between ventilation and increasing levels of activities

Lower level of activity=TV increase

Higher level of activity= RF increase
o Metabolic adaptations

VO2 max= CO x a-v O2 diff

VO2 max is most accurate indication of Cardio Respiratory fitness

Represents the maximum amount of O2 consumed per minute
Responses to conditioning
o Chronic adaptations to exercise results from a period of training

CV

Respiratory

Muscle metabolism
o Changes at rest

Decrease RHR

Decrease BP
o Changes with exercise

Decrease PR

increase SV

increase CO

increase max VO2

decrease myocardial O2 uptake
o respiratory changes at rest

increase lung volume

increase diffusion capacities
o respiratory changes with exercise

increase diffusion capacities

increase minute ventilation

increase ventilator efficiency
o muscle metabolism changes at rest

increase capillary density

increase mitochondria

increase muscle myoglobin
o muscle metabolism changes with exercise

decrease rate of glycogen depletion

decrease blood lactate levels

increase capacity to oxidize carbohydrates
factors which can modify response to exercise
o body size

volume of oxygen consumed per minute VO2 is strongly correlated with body weight

higher correlation with lean body mass
o Age

Decrease in maximal oxygen consumption

Decrease exercise CO

Decrease maximal exercise SV

Decrease in maximal exercise HR

Decrease respiratory function
o Maximum O2 consumption

Endurance capacity increase up to middle to late twenties

From 20-70 years of age , VO2 reduces

Trained individuals decline at a slower rate
o CO

Maximum decreases with age

Increased stiffness of myocardium and endocardium

Mitral valve thickens and calcifies-impedes ventricular filling

Increased size and thickness of peripheral vasculature
o HR

Max HR decreased (220-age)

Target HR-Karvonen formula

THR=max HR-RHR x % max HR+RHR
o SV

Progressive decreases with age

Increase afterload (aorta becomes stiffer)

Increased vascular resistance

SBP increases
o Respiratory changes

Decrease vital capacity

Increase respiratory frequency

Diffusing capacity decreases
o Gender

No differences between males and females during childhood

Following puberty, men have greater muscular and CR endurance
o Heredity

75% of biological variability is due to heredity factors

25% effected by training and deconditioning
o Initial fitness level

Conditioned vs. deconditioned

maximal O2 consumption

muscle function
o Types of exercise

UE vs. LE

UE more taxing; myocardial consumption is higher

Greater BP increases

See quicker rise in BP and HR

Angina threshold reached at lower workload with UE exercises

Isometric versus isotonic

Reactions to cold
o Peripheral vasoconstriction leading to increased peripheral resistance
o Coronary vasoconstriction can lead to angina
o Inhalation of cold air can lead to bronchospasm

Reactions to heat
o Vasodilation to subcutaneous tissue/skin
o Dehydration concerns
o Early signs and symptoms of angina may occur

Reactions to altitude
o Increased HR to maintain CO
o Increase RR-possible hyperventilation
o Angina levels may be reached sooner
Lecture #2 Cardiac Pathologies: ischemic Conditions and cardiac muscle dysfunction 1/13/15
Anatomy of Arteries

Tunica externa

Tunica media

Tunica intima

Basement membrane
Ischemic Conditions

CAD-obstruction that limits BF but no inhibition of heart muscle function
o Can lead to CHD
o 16 million Americans have a history of angina pectoris, MI, or both
o 1.5 million with have a MI each year
o 175,000 silent first attacks each year

CHD- obstruction that causes damage to heart muscle below inhibiting heart muscle function
o Number one killer of both men and women

Atherosclerosis: occurs at the intimal and endothelial linings of arterial walls and can lead to ischemia or
infarction
o Atherosis: fatty streaks; platelets aggregate; thrombus forms
o Sclerosis: responsible for decreased vessel compliance
o Pathogenesis

Normal artery

Endothelial lining is tightly packed cells allow for the smooth passage of blood

Protective covering against harmful substances circulating in the BS

Atherosis begins with an injury to the endothelial lining of the artery; vessel permeable to
circulating lipoproteins

Fatty streaks- lipoproteins penetrate the intima


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

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o
o
o
o
Chart:

A large fibrous plaque develops and impedes BF
Calcification with rupture or hemorrhage of the fibrous plaque
Thrombus may occur, occluding the lumen of the vessel
Normal—fatty streaks—atheromas—fibrous plaques—occlusion
What causes CHD? Cholesterol and fat, circulating in the blood, build up on walls of the
arteries
Vasospasm-atherosclerotic arteries are “prone” to spasm

Prinzmental/variant angina
o ST segment elevation (not depression)
o Occurs at rest (often in the a.m.; not with exertion)
o Not associated with increased myocardial VO2
o Relieved with NTG or vasodilator
o Exercise can help with vasospasm for vasodilation
Myocardial ischemia in CHD results from decreased perfusion of the cardiac muscles as
a result from reduction in coronary BF

Consequences of CHD that cause subsequent cellular damage

Reduced O2 supply

Inadequate removal of metabolites

Reduced nutrient supply
Risk factors of CHD (ischemia)

Major modifiable

Cigarette smoking

Hyperlipidemia

Hypertension

Physical inactivity

Minor modifiable

Age, gender, family Hx, race

Contributing factor

Obesity, response to stress, personality, diabetes, alcohol consumption,
hormonal status
Homocysteine-not yet a major risk factor by AHA

Amino acid related to higher risk of CAD stroke and PVD

Promotes atherosclerosis (by damaging the intima and promoting blood clots)

Folic acid and B vitamins help break down homocysteine
Clinical Course of CHD (ischemia)

Sudden death

Death within 1 hour or onset of sx

Typically it is the initial presenting syndrome

V-fib leads to decrease CO—death

Rx: emergency CPR

Preload is there but contractility is affected which increases afterload and
decreases stroke volume

Angina

Severe constricting pain the chest due to ischemia of the heart muscle

Etiology
o Narrowed arteries=compromised BF
o Cardiac workload is greater than O2 supply
o Supply/demand problem
o Insufficient myocardial O2

Four main triggers for angina
o Workload
o Stress
o Temperature= cold
o Overeating

Signs and Symptoms
o Substernal pressure
o Epigastric area; jaw, left shoulder/arm midscapular region
o Squeezing, tightness, crushing,; elephant on my chest
o Can be stationary
o If patient has pain in UQ then screen for CV deficiency

Types of angina

Chronic/stable angina
o Predictable
o Associated with some level of exertion
o Remember: Myocardial VO2= HR x SBP
o Rx: reduce intensity or activity, NTG (Vasodilator)

Unstable angina or infarction
o Sx in the absence of demands
o Lack of pattern of symptoms
o Progressive
o Higher mortality/morbidity rates
o You may be the profession al to determine “lack of pattern” to the sx
o Decompensated
o Clues for development of unstable angina

Sx of typical angina at lower levels of activity

Angina @ rest-biggest clue refer to PCP

Deterioration of previously status-decrease BP or increase
HR with previously well tolerated levels of activity

Prinzmetal’s (Variant) or vasospastic angina
o Angina produced from vasospasm of the coronary arteries in the
absence or with occlusive disease

Variant vs. unstable
o Variant is often relieved with low level of activity, often less severe
and the patient can perform higher levels of work later in the day
without discomfort
o Unstable is not relief with decreased activity, more severe, and the
patient is unable to increase CO without increases in Sx

Myocardial infarction
o Myocardial cell death resulting from complete occlusion of one or more coronary arteries (90100%)
o Usually people can function with 80% occlusion but will have angina
o Clinical presentation and prognosis is determined by the size and anatomic location of the area of
infarction
o Complications may include:

Arrhythmias, cardiogenic shock, pericarditis, extension of infarction, congestive heart
failure, sudden death
Cardiac muscle dysfunction

Most common cause of CHF

Impairs the ability of heart to pump blood

Impairs the ability of L ventricle to accept blood

Decrease in SV, decrease in CO, EDV increases, chamber is stretched out and impairs muscle function

Factors related to Ventricular performance
o Total blood volume
o Intrathoracic pressure
o Intrapericardial pressure
o Pumping of skeletal muscle
o Atrial contribution to ventricular filling
o Body pumping
o Venous tone

Factors that effect contractile state of myocardium
o Sympathetic nerve stimulation
o Circulating catecholamines
o Force-frequency relationship
o Digitalis/inotropic agents
o Pharmacologic depressants
o Loss of myocardium
o Intrinsic depression

Congestive heart failure (CHF)
o Group of clinical manifestations due to poor cardiac mm performance
o Results from increased fluid
o Heart attempts to maintain CO to the body
o






Described by which side of the heart is failing/injured

Right-sided CHF-cor pulmonae

Left-sided CHF- most common
o Fluid accumulates behind the lesion
o Systolic heart failure-impaired contraction of the ventricles during systole

Inefficient ejection of blood

Decrease ejection fraction (EF)
o Diastolic heart failure-inability of ventricles to accept blood
Causes of CMD/CHF
o HTN, CAD, Dysrhythmias, renal insufficiency, cardiomyopathies, valve abnormalities, pericardial
effusion, Pulmonary embolism/HTN, SCI, age related changes
Right failure manifestations (in the absence of left)
o Due to any pathology in the lungs (pulmonary stenosis, COPD, cystic fibrosis, emphysema)
o Decrease contractility of the right ventricle
o Backs up to periphery (jugular vein)
o Cyanosis
o Engorgement of jugular veins
o Hepatomegaly-enlarged liver
o Ascites (hard abdominal wall)
o Dependent edema
o Elevated venous pressure
o Cachectic-thin
Left heart failure manifestations
o Caused by breathing problems (dyspnea)
o Orthopenia-laying flat SOB
o No elevation of venous pressure
o Pulmonary edema
o Productive cough
o Fatigue
o Increase respiration
o Breathing effects
Treatment for CHF
o Dietary- decrease salt
o Pharmacologic
o Surgical
o Exercise training
o Ventilator muscle training
Hypertension- BP=Co x TPR
o Causes an increase in pressure load on the LV—LV hypertrophy
o Hypertrophy leads to increase myocardial VO2 (energy expenditure) due to increase myocardial
mass (heart has to work harder)
o LV becomes stiffer (decrease compliance) which loads L atrium
o Increase afterload=contractility is a problem
o Guidelines

Normal= <120/80

Prehypertension= 120-139/80-89

High stage 1= 140-159/90-99 stage 2=>160/100
o Clinical implications

Included as part of every PT eval

Must know BP responses to exercise and positional changes

Must know side effects and interactions of medications

Must know precautions and contraindications

Exercise has beneficial effects for patients with HTM
Coronary Artery Disease (CAD)
o Characterized by irregularity distributed lipid deposits in the intimal layer of arteries
o May result in MI, angina, myocardial ischemia, and or sudden death
o Clinical implications

Pt should bring sublingual NTG to PT

Monitor physiologic responses to activity

Communicate with PT regarding angina

Must know side effects and interaction of meds with activity

May have to modify PT Rx to include frequent breaks




Exercise training is beneficial
Cardiac arrhythmias
o Rapid or slow rhythms can impair function of the L/R ventricle—CMD
o May result from nodal dysfunction, heart blocks, tachycardia
o May be treated with meds, pacemaker, electrical cardioversion
o Any abnormal rhythm (fast, slow, unsynchronized) can impair atrial/ventricular function--- CHF
o Clinical implications

Physiological responses to activity should be monitored

Must know side effects and interactions of meds with activity

Exercise may be beneficial via improved ischemic threshold and or decreased
sympathetic nerve tone
Renal insufficiency
o Abnormal kidney function—volume overload
o Treatment

Diuretics to eliminate fluid from kidneys (must monitor electrolytes)

Dialysis (chronic state)
Cardiomyopathies
o Contractility is impaired
o Classified based on

Cause

Primary-in the heart itself

Secondary- due to systemic disease

Function

Dilated-ventricular dilation and cardiac muscle dysfunction
o Increase cardiac mass with little to no wall thickening
o Increase L VEDL and LVEDP---L dilation
o Decrease inergy available---decrease pumping
o Decreased SV and increase HR
o Progression- inability to maintain CO during exercise/movement
o Resultant- increase LVEDP---LV failure—RV failure
o Clinical manifestations

Dyspnea on exertion, then at rest

Nocturnal dry cough

s/s LV failure

chest pain on exertion

resting tachycardia

S3-S4 gallop

Cardiomegaly

Systolic murmur due to mitral/tricuspid regurgitation

Hypertrophic
o Increase cardiac mass without cavity dilation
o Diastolic dysfunction-impaires ventricular filling during diastole
o Increase LVEDP and subsequently L atria, pulmonary artery and
capillary pressures
o Results in disorganized hypercontractile myocardial muscle fibers
o Decrease LV compliance, rapid ejection, and increase ejection
fraction (should be 55-75% )
o Clinical manifestations

Dyspnea

Angina pectoris

Fatigue

Syncope

Palpitation

Loud S4 occasion PND (paradoxysmal nocturnal dyspnea)

Restrictive
o Diastolic dysfunction
o Caused by an endomyocardial disease
o Characterized by decreased ventricular filling and ventricular walls
rigis
o Clinical manifestations

Exercise intolerance

Weakness



o
o
o
o
o
o
Dyspnea
Increase CVP—JVD, edema, enlarged liver
Sx of CHF
Heart valve abnormalities

May cause CMD due to needed increased force to eject CO

Morecommon in the L vs R

Progression

Compensatory mechanisms
o Ventricular hypertrophy, chamber dilation, peripheral changes

Exhaust mechanisms—heart failure

Types

Valvular stenosis-typical, blocked

Valvular insufficiency-abnormal or poorly functioning valve leaflets

Valvular dysfunction four common terms

Atresia-congenital absence or closure

Prolapse-valve cusp falls back into the atrium during closure (mitral most
common)

Regurgitation- incompetent valve closure allows blood to flow backwards

Stenosis-valve becomes stiff-fibrotic; obstructs the passage of blood
Pericarditis

Inflammation of the pericardial sac surrounding the heart

Etiology: viral/bacterial infections, MI, trauma, TB, malignancy

May progress to pericardial effusion

Pericardial effusion- fluid accumulation in the pericardial sac

Lead to
o Cardiac compression
o Increase pericardial pressure
o Possible cardiac temponade
Cardiac tamponade

Compression of the heart

Characterized by:

Elevated intracardiac pressure

Decrease ventricular filling

Decrease SV

Decrease CO

Manifestations

Angina

Dyspnea

Pericardial friction rub

EKG abnormalities
Myocarditis-inflammation of the myocardial wall

Etiology

Strep infection

Viral

Bacterial

Funcgal

Parasitic

allergic

Manifestations

Fatigue

Dyspnea

Palpitations

Precordial discomfort- pressure on chest

Treatment- treat cause, rest
Pulmonary embolism

Obstruction of the pulmonary artery or one of its branches by an emboli

Elevates pulmonary artery pressure—increases RV work

Leads to decrease oxygenated coronary blood flow and blood flow to LV
SCI

Causes an imbalance in sympathetic and parasympathetic FB to the CV system

decrease sympathetic input, this prevents sympathetic changes

can lead to pulmonary edema

frequently fatal
o Diseases associated with CP function

HTN

DM

Obesity

PAD

Renal failure

Rhematic fever

Eating disorders
Lecture #3 Basic EKG theory and interpretation 1/20/15
Electrocardiogram- a record of the heart’s electrical activity

Records the electrical impulses that stimulate the heart to contract

These electrical impulses represent various stages of cardiac stimulation

Important information from EKG
o Heart rate and rhythm
o Cardiac ischemia- ST segment changes
o Cardiac hypertrophy- no change in amplitude
o Myocardial infarction- problems with the ST segment

Why do I need to learn to read an EKG
o Identify HR
o Determine the seriousness of an arrhythmia

Benign-continue intervention

Warning- reduce intensity

Life threatening- ventricle fibrillation and need to stop activity or code
o Determine appropriate action
o Look at text book for absolute vs. relative implications for stopping
Basic principles

When the heart is electrically stimulated it contracts

Rest= heart cells are charged/polarized (- inside; + outside)

Contraction = cells depolarize (+ inside; - outside)

Depolarization= advancing wave of positive charges within the cells

Depolarization causes progressive contraction of myocardial cells as the wave of positive charges advances
down the interior of the cells

Repolarization= myocardial cells regain negative charge within the cell

Repolarization is the electrical phenomenon and the heart remains physically quiet during this activity

EKG= records the electrical activity of depolarization and repolarization
Rule of electrical flow

If the electricity flows toward the negative electrode, the patterns produced on the graph paper will be
inverted

If the electricity flows toward the positive electrode, the patterns produced on the graph paper will be upright

P wave- atrial depolarization

QRS complex-ventricular depolarization; atrial repolarization

T wave- ventricular repolarization
Standard EKG

12 separate leads- usually used for diagnostic purposes
o 6 chest leads (V1-6)
o 6 limb leads (I, II, III, AVR, AVL, AVF)- intersect at 30 degrees and form 6 lines of reference in
the frontal plane (called axial reference system)

3 sets of leads
o limb leads (Einthoven’s)- each limb lead records from a different angle—different view of the
same cardiac activity
o augmented leads
o prechordial leads- chest leads sensor placed on chest is positive

VI, V2, V3 are placed posterior to anterior

V4, V5, V6 are placed right to left

Record electrical potential under the electrode compared to central connection

ECG becomes progressively more positive reflecting mass through which depolarization
passes
Conduction pathway of the heart

SA node—both atria stimulation—AV node---bundle of His---R and L bundle branches--- purkinje fibers--myocardial cells

SA node
o Located in the posterior wall of the R atrium
o Initiates electrical impulse for cardiac stimulation
o Depolarization stimulates both atria

Atrial stimulation
o Both atria contract concurrently
o Recorded as P wave
o < or = .11 seconds
o Bachman’s bundle- will stimulated the L atrium with the R

P-R interval
o
Beginning of P to the beginning of QRS complex
o represents the AV conduction time; atrial de/repolarization
o .12-.20 seconds
o pause at the AV node is recorded as the PR interval
o allows for ventricular filling

electrical impulse then reach the AV node= 1/10 second pause to allow blood to enter the ventricles

after 1/10 second pause, the AV node= stimulated, initiating electrical impulse that starts down the AV
bundle into the bundle of His

as the stimulus progresses away from AV node then it initiates ventricular depolarization (contraction)

the AV bundle (bundle of His) extends down from the AV nose and then divides into right and left bundle
branches within the interventricular septum

QRS complex
o
Represents depolarization/contraction of ventricles
o < or = .10 seconds
o purkinje fibers transmit the electrical activity of the stimulation of the ventricles
o R wave- the 1st upward wave of the QRS complex
o S wave- any downward wave preceded by an upward wave
o Q wave- the 1st downward deflection (may be absent on lead)

When > 25% entire height= pathology

ST segment- pause after the QRS complex
o If depresses= ischemia
o If elevation=acute MI

T wave- follows the pause
o Represents ventricular repolarization
Recording EKG’s

Orientation to paper
o Paper is marked by 1 mm square boxes
o Grouped by 5 by 5 squares with bolder lines demarcating the group
o Time on the horizontal axis

Each small box represents .04 sec

Each large box represents .20 sec

When paper speed is standard (25mm/sec)

1 min on horizontal axis= 300 large boxes and 1500 small boxes

6 sec= 30 large 150 small boxes
o Voltage is on the vertical axis

1mV displaces 10 mm or 2 large boxes

each small box= .1mV

amplitude is related to mass depolarizing; the larger the amplitude the greater the mass

PCP is looking for cardiac hypertrophy

Clinician is looking for ST segment changes

Interval times
o Normal PR interval

.12-.20 sec = 3-5 boxes

first degree heart block (>.2 sec) would have a wide PRI which would cause bradycardia

would not give person beta blocker and a pacemaker may be indicated if HR <40 bpm

<.12 sec would mean the patient was having tachycardia
o Normal QRS complex

.08-.10 sec =<2.5 boxes

determining HR
o
count how many beats per minute (R to R) there are in six second strip and multiply by 10

only accurate if the rhythm is regular
o count the number of small squares between two beats (each small square being .04 s) then divide
1500 by the number of small squares

there are 22 small squares between R to R so 1500/22=68 per minute
o count the number of large squares between 2 beats then divide 300 by number

there are 4 large squares between 2 beats so 300/4= 75 bpm
o quick count method

find R wave that occurs on dark line

300, 150, 100,75, 60, 50, 43
EKG interpretation

steps
o p wave- present or absent
o p wave regularity- regular or irregular
o PR interval- time from beginning of P wave until the beginning of the QRS complex (atrial
depolarization/repolarization)
o QRS- present or absent
o QRS- regular or irregular rate
o QRS interval- normal or abnormal
o T wave- elevation or depression

SA node normally sets the rate of the heart

If the pacemaker does not function normally, there are potential pacemakers available to take over the pace
setting activity (Ectopic Foci)

Ectopic pacemakers
o Only function in disease or emergency conditions
o Normal conditions- these are electrically quiet and do not function
o Possible locations: atria, AV node, Ventricles
o Atria ectopic pacemakers- may be faster or slower than normal
o AV node ectopic pacemakers- begins if normal stimulus fails to come form atria

Normal rate of AV node is 45-60 bpm
o Ventricular Ectopic pacemakers- rate of 30-40 bpm

Needs pacemaker
Rhythm interpretation (review in book)

Normal sinus rhythm
o HR- 60-100 bpm
o Rhythm- regular
o P wave- before each QRS identical
o PR interval- .12-20
o QRS- < .12

Sinus bradycardia
o HR- <60 bpm
o Rhythm- regular
o P wave- before each QRS, identical
o PR interval- .12-.20
o QRS- < .12

Sinus tachycardia
o HR- >100 bpm
o Rhythm- regular
o P wave- before each QRS identical
o PR interval- .12 to .20
o QRS- <.12

Atrial Flutter
o HR- A: 220-430 bpm V: <300 bpm
o Rhythm- regular or variable
o P wave- sawtoothed appearance
o PR interval- N/A cannot determine because don't know which one is firing SA node
o QRS- <.12
o one single eptopic foci

Atrial fibrillation- quivering of muscle fibers and can be many ectopic foci
o HR- A: 350 bpm V: slow to rapid
o Rhythm- irregular; r waves are consistently inconsistent
o P wave-fibrillatory (fine to course)
o
o
o









PR interval- N/A
QRS- <.12
Clinical implications

Etiology

Advanced age

Cardiac conditions

Digoxin toxicity

Renal failure

A serious rhythm, although stable

Potential for developing emboli

Anti-coagulant therapy
Ventricular tachycardia
o HR- <100
o Rhythm- regular
o P wave- absent not related
o PR interval- N/A
o QRS- > or equal to .12
o Clinical implications

Etiology: ischemia, acute MI, CAD, hypertensive heart disease, medication toxicity
(digitalis, quinidine for muscle cramping)

Symptoms- lightheadedness and syncope, weak and thread pulse

Emergency situation-decreased CO and BP

May progress to ventricular fibrillation and death

Treatment: meds, cardioversion, defibrillation
Ventricular fibrillation (can turn into asystole)
o HR-300-600 bpm
o Rhythm- extremely irregular
o P wave- absent
o PR interval- N/A
o QRS- fibrillatory baseline
Asystole (cardiac standstill)
o HR-absent
o Rhythm-absent
o P wave- absent or present
o PR interval- N/A
o QRS- absent
First degree Av blocks
o HR- before each QRS identical
o P wave- > .20- longer (not always alarming)
o QRS- >.12
o Characteristics- regular rhythm
third degree Av blocks (complete blocks)
o HR- normal but not related to QRS
o P wave- none
o QRS- N/A
o Characteristics- no relationship between P and RS
o will be on pacemaker to defibrillate heart
second degree AV blocks
o type 1- Block above AV
o type 2-Block below AV
right bundle branch block
o HR- before each QRS identical
o P wave- .12- .20
o QRS- >.12
o Characteristics- RSR in V1
left bundle branch block
o HR- before each QRS identical
o P wave- .12- .20
o QRS- >.12
o Characteristics- RR in V5
Premature contractions- initiated by ectopic foci
o
Types


Premature atrial complexes PACs

Ectopic focus in atria initiates an impulse before the next impulse is initiated in
the SA node

Underlying rhythm is sinus

P wave of the early beat is present; looks different than normal P wave’ may be
buried in the preceding wave

Etiology:
o Emotional stresses and infection
o Caffeine, nicotine and alcohol
o Hypoxemia, myocardial ischemia
o Rheumatic heart disease
o Atrial damage

Irregular pulse

If there are hemodynamic consequences, supraventricular tachycardia or atrial
fibrillation may develop
Premature Ventricular complexes PVCs

Ectopic foci originates an impulse in the myocardium of one of the ventricles

P waves are absent

QRS becomes “wide and bizarre

The ST and T waves are abnormal

A skipped beat can be palpated when checking pulse

PVC

Most common ventricular conduction abnormality

Benign or dangerous

May be making a patient ischemic as we cause them to exercise

It is very important that you identify immediately and decide on an appropriate
course of action

Etiology: caffeine/ nicotine
o Stress/overexertion
o Electrolyte balance
o Acid-base imbalance
o Cardiac diseases
o Irritation of myocardium
o Pharmacological toxicity
o Ischemia

Implications of PVS
o Of concern if ventricular ectopy increases with activity
o Increased activity= increased irritability
o 3 or more PVCs in a row=ventricular tachycardia
o increased irritability leads to dangerous arrhythmias
o ventricular tachycardia
lecture #4 EKG continued and cardiac procedures: lines, tests, and lab values 1/22/15
Recognizing Ischemia

Q wave changes
o Initial depolarization of ventricles
o Represents Myocardial necrosis if gets larger
o Duration < .3 seconds
o Normally appears in lateral leads (Lead I, AVL, V5, and V6)
o Abnormal if- the depth > .4 sec and or 25% the height of QRS complex

ST segment changes
o
Reflects early ventricular repolarization
o ST elevation =MI (acute)
o ST depression (> 1.5 mm)= ischemia

Upsloping (injury)- usually due to medications

Horizontal

Downslopping- cannot maintain CO

Ischemic triad
o Significant Q wave
o Elevated ST segment
o Inverted T wave
Indicators of acute MI
o
Presence of Q wave in the leads that normally don't have Q waves
o Q wave > 25% height of QRS
o Depression/inversion of ST segment- reduced blood flow to heart
o Injury- indicates acuteness of infarct
o ST segment elevation denotes injury
o ST segment is that segment of baseline between the QRS complex and the T- wave
Cardiac procedures: lines, tests, and lab values
Surgical procedures

Angiogram
o A radiographic record of the size, shape, and location of the heart and blood vessels
o Radio-opaque material is injected

Heart catherization
o
Sheaths are placed in both femoral artery and vein
o veins= access to R side of Heart
o arteries- access to L side of heart
o gives information on

blood flow

ejection fraction

chamber pressures
o pulmonary edema- R ventricular pressure
o CHF- L ventricular pressure
o Patient is usually on bed rest for 8-12 hours and will have hip precautions
o Need to be careful for sheath in hip
o No hip flexion past 30 degrees

PTCA- percutaneous Transluminal coronary angioplasty
o
Performed on more than 1 million people a year in the US
o purpose: to improve BF (revascularization)
o outcomes: improve sx of CAD (angina and SOB)

used during MI to restore BF
o balloon may have lysis drug on it to get rid of fat on the walls
o problems: stint can dislodge

Cardiac stenting

Coronary artery bypass graft (CABG)- use a vessel from another part of your body (leg, mammary area) to
“bypass” an area of ischemia or infarct
o Two types of CABG surgery

Traditional CABG- requires a median sternotomy, use a heart lung machine and
harvesting of saphenous veins for anastomosis

Used for multiple areas of occlusion

Mid CABG- MIDCAB does not utilize the heart lung machine or cardioplegia (stopping
the heart)

Small incision, avoids splitting the sternum

Uses mammary artery because only the distal end of the artery is cut

procedure is mainly used if patient is too weak for big surgery or if only one
artery is clogged
o Pump status

On- pump

heart stopped with cardioplegia and peripheral circulation occurs through
machine

Patients may experience lethargy, memory loss, and increased length of stays

Off-pump

Operating on beating heart

Pts experience better outcomes, shorter stays, and faster progressions

Used MIDCABs
o General surgical procedure for CABG

Midline chest incision

Chest tube- to accumulate any fluid in the chest

Pacemaker wires- usually used for a few days so heart can recover

Saphenous vein- bigger incision if emergency, smaller incision if planned
o General surgical procedure for MIDCAB



Minimally invasive revascularization surgery
Advantages

Less costly

Decrease risk of complications

Less trauma

Shorter operation, hospitalization, and recovery time

limitations

high risk patients

single artery involvement

Left ventricular assistive device
o Alternative to heart transplantation
o Provides bridge until suitable donor located
o Electrically powered device provides variability in pump output (dependent on patient’s
physiological needs)
o A progressive, monitored exercise program can improve pre-op condition

Heart transplant
o Indication- progressive terminal CP disease (Chronic CHF)
o Response to exercise (denervated heart)

Increased stroke volume—increased CO

No change in HR
Other Diagnostic Tests

Echocardiogram
o Evidence of MI
o Valvular function
o Ventricular function

Volumes

Ejection fraction

Ventricular hypertrophy

Areas of abnormal wall motion

Cardiac stress tests

Electrophysical studies
o Checks the conduction system of the heart:

After sudden death with revival

Runs of V-tech

WPW syndrome- wolf Parkinson white

Patient will have a chronic history of tachycardia due to ectopic foci

Heart blocks
o Patient is heavily sedated; procedure takes ~8 hours with pt. immobilized
o 2 large sheaths in femoral artery and vein on each side (4 total)
o MD inserts guide wires into the sheaths to electrically stimulate the heart
o Maps out the conduction system of the heart
Central Lines

Arterial line
o Locations

Femoral, brachial, radial
o Purposes

Measures arterial pressure

Used to draw blood

Invasive measurement of BP

Central venous line- placed in R atria
o Indications

Measure R atrial pressure

Peripheral venous access to:

Blood access

Medications

Rehydration

Placement of Swn-Ganz catheter

Swan-Ganz catheter- pulmonary artery catheterization
o Purpose- measure pressure R atrium, R ventricle, pulmonary artery, and L atrium filling pressure
o Normal values

Right atria- 0-5 mmHg




R ventricle- 5-12 mmHg
Pulmonary artery- 20-30/ 5-12 mmHg
Pulmonary capillary wedge pressure- 5-18 mmHg
Clinical tips
o Femoral artery versus vein sheath

Stand at foot of beed

Look at the involved groin

Consider “V-A”- vein is lateral and artery is medial

Always manually measure BP after moving a patient with “A line” or Swan Ganz line.
Machine calibration may be indicated
Peripheral lines

Intra-aortic balloon pump
o Mechanical cardiac assist device-assists L ventricular function
o Counter repulsion; reduces resistance to L ventricular ejection- increasing coronary blood flow

Basically acts as a suction to pull blood out of L ventricle
o Procedure

Sausage shape balloon is positioned in the descending thoracic aorta via the femoral
artery

Balloon inflated/deflated in synchrony with phases of cardiac cycle
o IABP Diastole

Aortic valve closure

Balloon inflated at onset of diastole—increase in aortic diastolic pressure

Displaces blood up toward aortic arch and down abdominal aorta (increases
coronary/systemic perfusion)

Benefits: increase in coronary, systemic, cerebral perfusion and potential to increase
coronary collateral circulatio
o IABP Systole- occurs prior to opening of aortic valve

Creates a vacuum that decreased aortic end diastolic pressure

Decreased impedance to L ventricular ejection

Benefits: decrease resistance to L ventricular ejection

Decreases L ventricular pre-load

Increased SV and CO
o Clinical tip

Patient may be fully oriented, with only ability to bend the hip

Therapeutic interventions:

ROM all extremities except LE involved

Cervical ROM

Education

Circulatory exercises

Hip precautions if sheath by groin
Intravenous lines

Most common in hospital

Indications
o Rehydration
o Administering of medications
o Blood transfusions

PICC Line- peripheral intravenous central catheter
o
Used for long term intravenous therapy

chemotherapy

antibiotic therapy
o advantages

easy to insert

low risk of bleeding

can be left in place for long periods of time
o non-invasive blood pressure cuff (NIBP)

correlates closely with arterial pressure

machine pump BP cuff

consult with RN before removing

remember to:

hit button before supine to sit; sit to stand
o
o
o

hit button after transitions for read out
pulse oximetry

resting= 98-100%

normal= 98-100%

no activity when= <92%

clinical tips

don't place probe on painted/false finger nails

be aware of decreased circulation
oxygen

most patient will be on O2 supplementation

consult with RN before ambulation

must be aware of how much O2

example:

if 3.0 L of O2 or less and o2 sats is > 95%- attempt exercise on room air

if patient tolerates room air by monitoring O2 sats >92%- attempt ambulation
on room air

if patient does not tolerate room air- perform ambulation with supplemental O2

if patient is on > 3 L/min of O2- may attempt to decrease flow and titrate O2
sats to 92% or greater

if patient doesn't tolerate decrease in flow and becomes symptomatic- leave O2
where it started

clinical tip

much of the Rx depends on pts condition

watch for signs of exertion like EKG changes, BP abnormalities, O2 sats

monitor vitals frequently

watch patient
lab values

enzymes-correlate with the amount of myocardial damage

when damage occurs to the myocardial tissue, intra-cellular enzymes are
released into circulation

enzyme levels increase within the first 36 hours after MI

CPK=creatine phosphokinase
o CPK-MB (myocardium iso-enzyme)

LDH= lactic dehydrogenase
o LDH-1= LDH-2 indicate myocardial damage

Troponin- indicates MI within ~ 7days
Lecture #5 PT examination and diagnosis of patients with cardiac dysfunction 1/27/15
Healing after an MI

Recovering from a heart attack takes time

Complete healing may take 4-6-8 weeks

The area of heart muscle damage is permanent

A firm scar replaces the damaged heart muscle and the remaining heart muscle takes over the work of
damaged area

Uncomplicated MI may go home within 1 week
o People with larger heart attacks or with complications may stay longer in the hospital

May perform low-level stress test prior to discharge

At home, patient will gradually increase ADL at home to normal over the next 2-4 weeks
o Client with sedentary office job may return to work after approximately 1-2 months
o Client with physical labor job is often advised to remain off work for 3 months

Angioplasty patients can drive within 24 hours
Medical/surgical history

Prior hospitalizations

Prior surgeries

Pre-existing medical and health-related condition

Secondary diagnosis and dates of events (ex: diabetes, amputation, ulcers, stroke, respiratory diseases)
Medications- all medications for all current conditions for which patient/client is seeking the services of a PT

Organic nitrates- NTG

Beta blockers- blocks signal; do not give to patients with bradycardia

Calcium channel blockers


Antihypertensive- Ca channel blockers
Angiotension converting enzyme inhibitors (ACE)- prevent angiotension I from converting into
angiotesion II which is a major vasoconstrictor

Antirrhythmics

Cardiac glycosides- ionotrophic drugs

Anti-lipidemic agents- statin (lipitors)

Anti-coagulation agents- warfarin

Insulin, hypoglycemic agents
Social/Health habits

Look for past and current level of fitness (past and immediately pre-event exercise history)

Risk factors
o Smoking
o history of HTN, obesity, stress
o history of hyperlipidemia
o family history of coronary artery disease and diabetes
o eating and drinking habits
o non-modifiable- family history, gender, age, ethnicity
o modifiable- HTN, hyperlipidemia (high cholesterol, high LDL and low HDL), smoking, diabetes,
obesity, inactivity, stress
o emerging- metabolic syndrome, homocysteine, CRP, microalbuminuria, hypercoagulable states,
inflammatory conditions, increased clotting factor VII

Hypertension
o Ideal blood pressure 120/80
o Pharmacological intervention when BP reaches 140/90
o In case of DM, intervention is appropriate at 130/80

Hyperlipidemia
o Elevation of the total blood cholesterol

80% of the body’s cholesterol is produced internally

20% is related to diet
o risk of MI relatively low with total cholesterol levels less than 200
o total cholesterol in the 220-250 range have twice the risk of MI

LDL-Cholesterol
o
Better predictor of MI risk than total blood cholesterol
o high risk:160-189
o borderline: 130-159
o optimal: <100
o
in the presence of heart disease, stroke, vascular disease, aneurysm or type two DM, the ideal LDL
cholesterol is less than 75

HDL cholesterol
o Men: >40
o Women: >50
o Behaviors that raised levels of HDL include weight loss, smoking cessation, and increased aerobic
exercise
o Elevated triglycerides also reduce HDL cholesterol and thus, increased the risk of MI

Fasting triglyceride levels above 200 are considered elevated

Metabolic syndrome
o
A cluster of risk factors
o elevated triglycerides: >150
o low HDL: <50
o obesity waist circumference: >35 in
o hypertension: 130/85
o impaired blood glucose: fasting >100

CRP (C-reactive protein)
o A marker of vascular inflammation
o A strong predictor of future CV events
o Risk levels

Low risk is defined as hs-CRP (high sensitivity-CRP) < 1

average risk: 1.0-3.0

high risk: 3.0-10
o useful test to predict CV risk particularly in patient with low LDL levels and the absence of other
traditional cardiac risk factors

Family history
o Familial health risks
o Relationships following injury
o Making sure you get a perception on what they are clinically going through

Laboratory
o Enzymes
o Blood studies

Diagnostic studies
o Catheterization (angiograms)
o Echocardiograms
o X-rays
o Thallium scans
o Exercise stress test
Systems review

Tests and measures
o 6 minute walk test is the standard predictor of mortality and morbidity
o phase three would include a 1 mile walk test
o others-SEE SLIDES
o Aerobic capacity and endurance

Physiological monitoring at rest and in response to activity

Performance or analysis of ECG

Monitoring via telemetry during activity

Clinical endurance testing

Timed/distance walking/wheeling/cycling tests

Assessment of performance using established exercise protocols

(e.g. treadmill, ergometer)

Exercise testing-General overview
o non-invasive test measuring CV and pulmonary response to increased activity
o can be performed safely by properly trained nurses, exercise physiologists, PA, PT or medical
technicians
o must be supervised by an appropriately trained physician
o Indications

Diagnosis-CAD, HTN, pulmonary conditions

Assessment- evaluation of arrhythmias, dyspnea, ability to work, evaluation of medical
and surgical interventions

Prescription of exercise program

Screen to provide prescription

Provide motivation for lifestyle change

Decrease risk of CAD
o Modes

Informal methods

12 minute walk test

cooper’s 12 minute run

1.5 mile run

Formal methods

Step test

Treadmill-ideal because it is more specific

Bicycle

Upper extremity arm or wheelchair ergometry
o Intensity

Submaximal

Predetermined maximum heart rate as end point

Absolute or % predicted max heart rate (PMHR)

Maximal

Symptom limited maximum until pt. perceives inability to continue (SOB, leg
fatigue, or chest discomfort)
o Continuous vs. intermittent

Continuous- incrementally progressive workloads until test is terminated

Intermittent- progressive workloads with short rest periods
o Treadmill protocols

Bruce protocol- most commonly used clinically

SEE PPT FOR GRAPH EXAMPLE
Balke protocol- most commonly used with athletes
Exercise capacity should be reported in estimated metabolic equivalents (METs0 of
exercise
Monitor! HR, BP, EKG, and subjective ratings (RPE, angina scale, dyspnea scale)
Data collected

Duration

BP, HR

Symptoms-fatigue, angina, claudication, dizziness

EKG derived data- HR, arrhythmias, ST segment changes

Expired gases- O2 consumption, CO2 production, pulmonary function
Criteria for termination

Absolute

Drop in SBP >10mmHg

Moderately severe angina

Signs of poor perfusion

Sustained V-tachy

Patients request

Relative

ST or QRS changes

Arrhythmias

Fatigue, SOB, claudication

Increasing chest pain

Hypertensive response (SBP >250; DBP >115)
Interpretation

HR response

BP response

EKG data

Heart sounds

Assessment of aerobic capacity

METs achieved

functional aerobic impairment (FAI)


o
o
o
o





Level of impairment
Percent of FAI
Mild
27-40%
moderate
41-54%
Marked
55-68%
Extreme
>68%

contraindications to testing
o recent MI
o acute pericarditis
o resting or unstable angina
o aortic stenosis
o serious ventricular or rapid atrial arrhythmias
arousal, attention and cognition
o assessment of orientation to time, person place, and situation
o screening for cognition: determine ability to process commands, to measure safety awareness
o communication
o motivation
o recall that some patients may have sustained periods of hypoxia
assistive and adaptive devices- analyze effects and benefits of DME and evaluation energy
conservation/expenditure
circulation
o cardiovascular signs-HR, rhythm, BP, claudication, EKG
o cardiac symptoms in response to activity
o volume/girth measurement
gait, locomotion and balance- physiological response during gait- HR, BP, symptoms, heart sounds
integumentary assessment
o assessment of nailbeds








clubbing involves a softening of the nail bed with the loss of normal angle between the nail
bed and the fold, an increase in the nail fold convexity, and a thickening of the end
of the finger so it resembles a drumstick

80% of clubbing is due to cardio-pulmonary causes

schamroth’s sign- to determine whether nails are clubbed, have the patient place both
forefinger nails together and look between them. If you see a small diamond space
between them, clubbing is not present
assessment of open chest wound
o be cautious of UE motion
o for CABG grafts make sure look at lower leg during assessment
pain
o assessment of muscle soreness
o chest pain description and differentiation
o note patient’s present complaint and onset of symptom and characteristics
symptoms of angina
o the symptoms include a heavy or constricting feeling in the chest
o increasingly short of breath when they exercise
o may be accompanied by nausea or dizziness
o the type of pain caused by angina is continuous, not stabbing
o The angina scale

1+- light, barely noticeable

2+- moderate, bothersome

3+- severe, very uncomfortable

4+- most severe pain ever experienced

make sure to not location and distribution of pain along with the intensity at its onset and
duration
Rating of perceived exertion
o 6-20- based on 60 bpm to 200 bpm
o 11-13 is light to somewhat hard
o 9-corresponds to very light exercise. For a healthy person it is like walking slowly at comfortable pace
for some minutes
o 13-osomewhat hard exercise by still ok to continue
o 17- very hard and healthy person can still go on by has to push themselves. It feels very heavy and the
person is tired
o 19-extremely strenuous exercise level. For most people is is the most strenuous exercise they have ever
experienced
o Modified Borg scale: 0-10

A rating of 3-5 is considered adequate for a training
Ventilation, respiration (gas exchange)- patient’s present complaint, description of his symptoms like breathing,
fatigue, vertigo, claudication
o Function Dyspnea scale
 0- not troubled with breathlessness except with strenuous exercise
 1- troubled by shortness of breath when hurrying on the level or walking up a slight hill
 2- walks slower than people of the same age on the level because of breathlessness or has to
stop for breath when walking at own pace on the level
 3- stops for breath after walking about 100 meters or after a few minutes on the level
 4- too breathless to leave the house or breathless when dressing or undressing
o Dyspnea level- able to count to 15 in a 7.5-8 second period
o
Level 0- on a single breath
o
Level 1- requires two breaths
o
Level 2- requires three breaths
o
Level 3- requires 4 breaths
o
Level 4- unable to count
Evaluation- a dynamic process in which the PT makes clinical judgments based on data gathered during the
examination
Diagnosis- the process and the end result of evaluating information obtained from the examination data, which the
PT organizes into defined clusters, syndromes, or categories to help determine the prognosis and the most
appropriate intervention strategies
Lecture #6 PT Intervention Cardiac Rehabilitation 1/29/15
Phases of cardiac rehabilitation

Phase I: acute phase- monitoring phase
o
o
o
o
o
Multidisciplinary Team

Cardiac rehab specialist-oversees education and referrals for risk factor modification

Physical therapist- “ early mobilization” to decrease effects of prolonged bed rest

Identifying which daily activities can be done safely

Information of rehab options after discharge

OT: Self care (bathing, dressing, and grooming)

Dieticians- recommendations for dietary changes to reduce risk factors (low fat, low
cholesterol, high fiber and limited salt diet)
Phase I in CHF patients

SOB

persistent cough

excessive fluid

fatigue

lack of appetite

confusion

increased HR at rest
sample activity progression for CHF patient

step 1- rest in bed until stable; sit up in be with assistance; stand at bed with assistance;
perform self care activities while seated; march in place; weight shift

step 2- sit up in bed independently; walk in room and to bathroom; perform self care
activities in bathroom

step 3- sit and stand independently; walk in hall with assistance; 5 to 10 minutes, 2 to 3
times a day

step 4- walk in hall; 5 to 10 minutes , 3 to 4 times a day; walk up and down a flight of
stairs with assistance (PRM)
Phase I: post-op patient

CICU or MSICU---TICU---cardiology unit (telemetry unit)

average length of stay- 5 days

cardiac rehab begins on 1st or 2nd day
sample activity progression for Post op patient

1st and 2nd days post-op

reinforce breathing exercises with incentive spirometry (x10 per day),
coughing techniques

bed mobility—OOB (relieve pressure)

goal is to sit in chair several times a day

gentle LE exercises

monitor O2 sats

3rd and subsequent days post op

ambulate 2-3x day

independent in personal hygiene

stair climbing before d/c

Sternal precautions

Avoid pressure on the sternum

Encourage splinting chest with pillow when coughing

Avoid bilateral shoulder flexion, abduction >90 degrees

Do not allow patient to use arms for resisted activity

Avoid activities that may cause valsalva maneuver

No driving and no sitting in passenger seat behind airbag for 4 weeks

Harvest site considerations

WBAT for both LE

No ROM restrictions given normal healing

The patients shoulder wear thigh high TEDs with ambulation

Elevate involved LE

Perform frequent LE AROM when sitting for prolonged periods of time

Avoid crossing of legs (ankles or knees)

Typical pathway progression

Day 0- bed rest with HOB—30 degrees as tolerated OOB or chair position up
to 2-4 hours after extubation for up to 2 hours

Day 1- OOB in chairs BID

Day 2- ambulate in room with assistance; exercise program



Day 3- ambulate in room and hallway with assistance as needed; exercise
program

Day 4- ambulate without assistance; exercise program

Day 5- ambulate up and down stairs as indicated; may shoulder without
assistance
Phase II: subacute phase- conditioning phase
o Purpose of the phase

Increase exercise capacity and endurance in a safe and progressive manner

Ensure continuity of the exercise program with a transition of home environment

Assess the CV response of mild to moderate workloads

Teach the patient to apply techniques of self-monitoring to home activities

Obtain monitored objective on medication effectiveness

Relieve anxiety and depression

Increase patient’s knowledge of disease process and how personal health habits affect

Promote positive lifestyle changes

Easily influenced and educated at this time due to fear and anxiety about health and
longevity
o Exercise prescription

Mode

Stationary biking and walking
o Common, continuous utilization of large muscle groups
o Allow EKG monitoring

Circuit-interval training
o Allow pts to work at higher intensities
o Exercise at a lower rate of perceived exertion

Low-level weight training
o Should be incorporated gradually
o 1-2 pounds for UE

intensity

Initially 40-60% of maximal heart rate

Patients demonstrating appropriate CV responses to training during the first 2-3
weeks can be progressed by increasing the target HR by 10 bpm each week
therafter

Frequency

Generally 3x/ week under supervision

Home exercise sessions: 1-2 weeks

5-6 session of exercise per week is recommended

duration

initial duration of 10-15 minutes continuous low-level exercise

emphasis is on progressing to 30-45 minutes of LE continuous and 10-15
minutes of UE continuous exercise during weeks 2-4

important: include warm-up and cool down

Discharge Criteria

Medically stable, no longer require EKG monitoring

Independence in self monitoring

Compliant with HEP

Maximum symptom-limited exercise test administered (MD usually performs)

Encouraged to continue structured rehabilitation by participating in Phase III
program
Phase III and IV: training phase- intensive rehabilitation and prevention program
o Conditioning and community phases
o Variable length
o Intermittent to no EKG monitoring
o Under supervision to limited supervision
o Purposes

Provides the coronary patient with the opportunity to achieve a higher level of physical
and mental functioning

Provides incentives for the patient to continue the lifelong habit of exercise, risk factor
reduction and on-going education

Provides mechanism for serial re-evaluation to asses progress and disease stability
o Goals
o
o
o
o
o
o
o
o




Mode



Improve physical fitness and endurance level
Produce long term reduction in risk factors
Improve patient’s knowledge of disease and role in health maintenance
Improve/enhance patient’s quality of life
Aerobic activity involves large muscles
Rhythmic and dynamic
Common modes:

Walking, brisk walking, jogging, bicycling, swimming, aerobics, dancing, x
country skiing, rowing, bench stepping, stair climbing, jogging, flights of stairs,
UE ergometer, rope jumping
Special considerations

Strength training

Specificity of training

UE vs. LE exercise

Oxygen uptake, HR, and systemic blood pressure are greater during arm
exercises than leg exercises at the same submaximal workloads

Myocardial oxygen consumption is higher with arm exercises

Coronary patients complete 35% less work with arm exercises before
symptoms occur
Intensity

Recommended conditioning intensity for asymptomatic persons in between 60 and 70%
of functional capacity (70-85% max HR, 60-75% HR reserve)

Intensity may be prescribed by either HR, METS, RPE
Determining exercise HRs (see slides for examples)

Estimated maximum HR: 220- age

Target HR- maximum estimated HR x desired level

Karvonan’s formula- max(estimated HR-RHR x desired workload+ RHR)
Determining exercise RPE

May be given overestimated initially (higher RPE’s are given for a specific HR) but with
training the values normalized

Especially useful when evaluating patients on beta blocking or Ca channel blocking
medications

Cautions must be used with aggressive, competitive personality who deny that they
perceive exertion to be “hard”
Energy cost of various activities

1-2 METS- standing strolling 1mph

2-4 METS- self care, walking 2 mph, level bicycling 5mph, bowling, fishing,
calisthenics, gold using cart

4-6 METS- walking 4 mph, moderate housework, bicycling 10 mph, table tennis,
golfing, social and square dancing, fishing by wading in stream, golf walking carrying or
pushing bag

6-8 METS- jogging 5 mph, bicycling 12 mph, hill climbing, downhill skiing

8-10 METS- running 6 to 9 mph, mountain climbing

10-12 METS- swimming > 40 yds, basketball, racquetball
Duration: goal: 20-30 minutes if moderate intensity; 40-60 minutes if low intensity

When time period is not available, try a number of 10-15 min. periods throughout the day

Greater durations are necessary when training at lower intensities to achieve conditioning
effect

Longer duration, lower intensities to achieve conditioning effect

Longer duration, lower intensity exercise is recommended if the patient goals are

To reduce body fat

Relieve intermittent claudication

Control hypertension
Frequency

Frequency of exercise is dependent on the intensity and duration at which the individual
is able to exercise continuously

3 to 5 exercise sessions a week at moderate intensity and duration is generally
accepted for maintaining or improving levels of conditioning

if continuous exercise duration is <15-20 minutes, frequency should be 2-3 times/day

if continuous exercise duration is >20 minutes frequency can be once a day 3-7
days/week depending on the intensity


low to moderate: 5-7 days/week
higher intensity: 3-5 days / week