Stress testing

&
ECG
POONAM SONI
ROLL NO. 210172690005
WHAT IS STRESS TESTING
Tests used in Medicine to measure the heart’s ability to respond to external stress in a controlled
clinical environment
TYPES OF STRESS TESTING
1. EXERCISE
a. Treadmill
b. Bicycle

2. PHARMACOLOGIC
a. Adenosine
b. Dipyridamole
c. Dobutamine
d.Isoproterenol
3.OTHER

a.Pacing

INDICATIONS OF EXERCISE TESTING

• Elicit abnormalities not present at rest

• Estimate functional capacity

• Estimate prognosis of CAD

• Likelihood of coronary artery disease

•Extent of coronary artery disease

•Effect of treatment

INDICATIONS OF PHARMACOLOGICAL STRESS TESTING

 Patients inability to exercise adequately because of physical or psychological limitations.
 The chosen test cannot be performed readily with exercise (e.g. PET scanning).

METHODS OF DETECTING ISCHEMIA DURING STRESS TESTING

 Electrocardiography
 Echocardiography
  Myocardial perfusion imaging
 Positron emission tomography
 Magnetic resonance imaging
ACC/AHA GUIDELINES (American College of Cardiology/ American Heart
Association)

Indications for exercise testing to diagnose obstructive coronary artery disease Adult
patients with right bundle branch block or less than 1mm of resting ST depression with an
intermediate pretest probabilty CAD on the basis of gender , age and symptoms.
Indications in patients with prior history of coronary heart disease

 Patients undergoing initial evaluation with suspected or known CAD, including those
with complete right bundle branch block or less than 1mm of resting ST depression.
 Patients with suspected or known CAD , previously evaluated , now presenting with
significant change in clinical status .
 Low risk (on pretest probability), unstable angina patients 8 – 12 hours after presentation
who have been free of active ischemia or heart failure symptoms.
 Intermediate risk (on pre test probability),unstable angina patients 2 to 3 days after
presentation who have been free of active ischemic or heart failure symptoms.

Indications in patients with Valvular heart disease

 In Chronic Aortic Regurgitation for assessment of functional capacity and symptomatic

responses in patients with a history of equivocal symptoms.
 . Aortic stenosis – role of exercise testing in asymptomatic AS patients , with
recommendations that aortic valve replacement be considered in those with exercise
induced symptoms or abnormal blood pressure response.
 Mitral stenosis – class 1 reommendation for stress echocardiography in patients with MS
and discordance between symptoms and stenosis severity.
 Threshold values proposed for consideration of intervention:
a. Mean transmitral pressure gradient >15 mm Hg during exercise.
b. A peak pulmonary artery systolic pressure > 60 mm Hg during exercise.
 Mitral regurgitation – In asymptomatic patients with severe MR, exercise stress echo
helps identify:
a. Patients with subclinical latent LV dysfunction
b. Worsening of MR severity
c. Marked increase in pulmonary arterial pressure
d. Impaired exercise capacity
  Prosthetic heart valves – Stress echocardiography used in confirming or excluding the
presence of hemodynamically significant prosthetic valve stenosis or Patient prosthesis
mismatch (PPM).

RHYTHM DISODERS

Evaluation of congenital complete heart block in patients considering increased physical activity
or participation in competitive sports .

CONTRAINDICATIONS FOR STRESS TESTING

 Acute myocardial infarction ( within 2 days )
 High risk(on pretest probability) unstable angina
 Uncontrolled cardiac arrthymias causing symptoms or hemodynamic compromise
 Symptomatic severe aortic stenosis
 Acute pulmonary embolus or pulmonary infarction
 Acute myocarditis or pericarditis
 Acute aortic dissection

EXERCISE PHYSIOLOGY
 Patient position – supine or upright.
 At rest CO and SV more in supine position than in upright position
 Change from supine to upright position causes , CO as a result of in SV and HR.
 The net effect on exercise performance is an approx. 10 % increase exercise time
cardiac index, heart rate, and rate pressure product at peak exercise in the upright as
compared with the supine position.
 The main types of exercise are isotonic or dynamic exercise, isometric or static exercise,
and resistive (combined isometric and isotonic) exercise.
Isometric
a. Holding a static pushup position;
b. Holding a dumbbell in one hand;
c. Pushing against an immovable object, such as a wall.
Isotonic
a. Weight lifting
b. Swimming
c. Rock climbing
d. Cycling
CARDIOPULMONARY EXERCISE TESTING
 Involves measurements of respiratory oxygen uptake (VO2),carbon dioxide production
(VCO2), and ventilatory parameters during a symptom-limited exercise test.
 VO2 max is the product of maximal arterial-venous oxygen difference and cardiac
output and represents the largest amount of oxygen a person can use while performing
dynamic exercise involving a large part of total muscle mass.
 The VO2 max decreases with age, is usually less in women than in men, and diminished
by degree of cardio-vascular impairment and by physical inactivity.
 Peak exercise capacity is decreased when the ratio of measured to predicted VO2 max is
less than 85 to 90 percent.

METABOLIC EQUIVALENT

 Metabolic equivalent (MET) refers to a unit of oxygen uptake in a sitting, resting

person.
 1 MET is equivalent to 3.5 VO2 ml 02/kg/min of body weight. Measured VO2 in ml
02/kg/min divided by 3.5 ml 02/kg/min determines the number of METs associated
with activity.
 Work activities can be calculated in multiples of METs; this measurement is useful
to determine exercise prescriptions, assess disability, and standardize the reporting of
submaximal and peak exercise workloads when different protocols are used.

Methods

General concerns prior to performing an exercise test include –

 Safety precautions and equipments needs.

 Patient preparation
 Choosing a test type
 Choosing a test protocol
 Patient monitoring
 Reasons to terminate a test
 Post test monitoring

SAFETY PRECAUTIONS AND EQUIPMENT

 The treadmill should have front and side rails for subjects to steady themselves.
 It should be calibrated monthly.
 An emergency stop button should be readily available to the staff only.
 Exercise test should be performed under the supervision of a physician who has been
trained to conduct exercise tests.
PRETEST PREPARATION

 Any history of light headed or fainted while exercising sholud be asked.

 The physician should also ask about family history and general medical history, making
note of any considerations that may increase the risk of sudden death.
 A brief physical examination should always be performed prior to testing to rule out
significant outflow obstruction
 The subject should be instructed not to eat or smoke atleast 2 hours prior to the test .
 Unusual physical exertion should be avoided before testing.
 Specific questioning should determine which drugs are being taken. The labeled
medications should be brought along so that medications can be identified and recorded.
 Because of a greater potential for cardiac events with the sudden cessation of –blockers ,
they should not be automatically stopped prior to testing but done so gradually under
physician guidance, only after consideration of the purpose of the test.

EXERCISE PROTOCOLS
 Dynamic protocols most frequently are used to assess cardiovascular reserve, and those
suitable for clinical testing should include a low intensity warm-up phase.
 In general, 6 to 12 minutes of continuous progressive exercise during which the
myocardial oxygen demand is elevated to the patient’s maximal level is optimal for
diagnostic and prognostic purposes. The protocol should include a suitable recovery or
cool-down period.

VARIOUS PROTOCOLS

Treadmill protocols

a. Bruce

b. Cornell

c. Balke ware

d. Acip

e. mAcip

f. Naughton

g. Weber
Bicycle ergometer
TREADMILL PROTOCOL
 In healthy individuals, the standard Bruce protocol is normally used.
 The Bruce multistage maximal treadmill protocol has 3-minute periods to allow
achievement of a steady state before work-load is increased for next stage.
 In older individuals or those whose exercise capacity is limited by cardiac disease, the
protocol can be modified by two 3-minute warm –up stages at 1.7 mph and 0 percent
grade and 1.7 mph and 5 percent grade.

The 6-Minute Walk Test

 Used for patients who have marked left ventricular dysfunction or peripheral arterial
occlusive disease and who cannot perform bicycle or treadmill exercise.
 Patients are instructed to walk down a 100-foot corridor at their own pace, attempting to
cover as much ground as possible in 6 minutes.
 At the end of the 6-minute interval, the total distance walked is determined and the
symptoms experienced by the patient are recorded.

MEASUREMENTS

 ECG
 Exercise capacity (METS – metabolic equivalent)
 Symptoms
 Blood pressure
 Heart rate response & recovery

Positive test

a. A flat or downsloping depression of the ST segment > 0.1 mV below baseline (i.e the PR
segment ) and lasting longer than 0.08s

b. Upsloping or junctional ST segment changes are not considered characteristic of ischemia

and do not constitute a positive test.

Negative test

a. Target heart rate (85% of maximal predicted heart for age and sex ) is not achieved .

MAXIMAL WORK CAPACITY

 In patients with known or suspected CAD, a limited exercise capacity is associated

with an increased risk of cardiac events and in general the more severe the limitation,
the worse the CAD extent and prognosis. In estimating functional capacity the
 amount of work performed (or exercise stage achieved) expressed in METs and not
the number of minutes of exercise, should be the parameter measured. Major
reduction in exercise capacity indicates significant worsening of cardiovascular
status.

BLOOD PRESSURE RESPONSE

 The normal exercise response is to increase systolic blood pressure progressively

with increasing workloads to a peak response ranging from 160 to 200mmHg with
the higher range of the scale in older patients with less compliant vascular systems.
 Failure to increase systolic blood pressure beyond 120mmHg or a sustained decrease
greater than 10mmHg repeatable within 15 seconds or a fall in systolic blood
pressure below standing resting values during progressive exercise when the blood
pressure has otherwise been increasing appropriately, is abnormal .

HEART RATE RESPONSE

 Peak HR > 85% of maximal predicted for age } HR recovery >12 bpm (erect) } HR
recovery >18 bpm (supine)
 Chronotropic incompetence is determined by decreased heart rate sensitivity to the
normal increase in sympathetic tone during exercise and is defined as inability to
increase heart rate to atleast 85 percent of age predicted maximum. Heart rate reserve is
calculated as follows – % HRR used = (Hrpeak- Hrres) / (220-age-Hrres) Abnormal
heart rate recovery refers to a relatively slow deceleration of heart rate following exercise
cessation. This type of response reflects decreased vagal tone and is associated with
increased mortality.

LIMITATIONS OF TREADMILL STRESS TEST

 Non-diagnostic ECG change
 Women – false positives
 Elderly – more sensitive/less specific
 Diabetics – autonomic dysfunction
 Hypertension } Inability to exercise
 Drugs – digoxin; anti-anginals
Electrocardiography (ECGs)
BASIC ELECTROPHYSIOLOGY
Heart cells, when they are not beating, are polarised - that is, the electrical charge on the outside
of the cell membrane is positive compared with the inside. Contraction of the heart muscle is
triggered off by depolarisation of the cell membrane; that is a movement of ions (initially sodium
and later mainly calcium) across the membrane so that the polarity is reversed and die interior of
the cell is positive compared with the exterior. Once depolarisation has started it spreads
throughout the heart from cell to cell to ensure a synchronised heart beat. Depolarisation is
followed by a recovery phase - repolarisation - and following this the cell membrane remains
stable until depolarization occurs again. Certain cells in health, e.g. in the sinuatrial (SA) node,
will depolarise spontaneously and initiate the heart beat, while other cells will only do so under
pathological conditions. The wave of depolarisation, followed by repolarisation, create voltage
changes that can be picked up at the skin and it is a recording of these voltage changes that make
up an electrocardiogram. Once depolarised, muscle cells are incapable of transmitting a further
impulse until they are repolarised. During this time when they cannot be stimulated they are said
to be refractory.

CONDUCTION IN TtlE NORMAL HEART BEAT

Normally the cardiac impulse arises from the sinuatrial node, a group of specialised cells in the
right atrium near the mouth, of the superior vena cava. The impulse spreads from here through
the atria rapidly to reach the atrioventricular node. Conduction through the atrioventricular node
is slower. The impulse then travels to the ventricle by specialised conduction tissue, the bundle
of His, which divides into two branches - the left and right bundle branches supplying the left
and right ventricle. The left bundle branch in turn divides into superior and inferior fascicles
supplying different areas of the left ventricle. The bundle branches connect to Purkinje fibres
which lie on the endocardial surface of the heart. The impulse therefore reaches the endocardial
surface of the heart nearly simultaneously. The excitation wave then spreads from endocardium
towards the epicardial surface travelling through contractile muscle cells. The anatomy of the
conducting tissue ensures that all parts of the ventricle contract at about the same time. Voltages
generated in the sinuatrial node, atrioventricular node and specialised conducting tissue are not
large enough to be detected by
conventional electrocardiography. The electrocardiogram therefore
records voltage changes associated with conduction in the atrium and
the ventricle.
LEADS
By convention, electrodes are placed on nine points on the skin (+ one
additonal position used to earth the machine). From these electrode positions it is possible to
derive 12 separate tracings. Each of these can be considered to represent a view of the heart’s
electrical activity from a different direction.
Lead I represents voltage change in the frontal plane pointing to the left (upright on the ECG
tracing) and to the right (downwards on the tracing.) Lead aVF represents voltage changes in the
frontal plane pointing downwards (upright on the tracing) or upwards (downwards on the
tracing). Leads II, III, aVL and aVR also represent voltagechanges in the frontal plane, the
direction of the arrow being positive, i.e. upright on the tracing. Leads Vi to V6 represent voltage
change in the horizontal plane. The direction of the
arrows is positive. Leads Vi and V2 look at voltages moving anteriorly and posteriorly. V6
mainly shows voltage moving to the left and right and so is similar to lead I.

Position of electrodes on the body: left wrist; right wrist; left ankle; 6 leads on the chest
wall from the 4th intercostal space to the left midaxillary line; (right ankle lead is the
earth).
TRACING
The changes in voltage are traced on paper running at the speed of 25mm/second. Voltage
change is on a scale of icm = 1 millivolt.
 Stylised ECG tracing of one heart beat

By convention the waves are named after the following letters:

P wave represents atrial activity.
QRS represents ventricular activity.
R wave is the first positive wave.
Q wave is a negative wave not preceded by R.
S is a negative wave following an R.
T wave represents electrical changes which occur following the contraction when the muscle
‘repolarises’ in preparation for the next heart beat.

Interpretation of the normal electrocardiogram

Electrocardiography is not an exact science. The correlation between ECG findings and the
anatomical and physiological state is not perfect. Interpretation should be both empirical and
deductive. Empirical is purely noting that a certain pattern is associated with a certain condition.
Deduction implies analysis of the ECG pattern with regard to the temporal sequence of events
and the direction of electrical activity.
Atrial activity spreads from the sinus node to the atrioventricular node (P wave). The effective
direction of the impulse is downwards, to the left and tb the front. That means that normally the
P wave is positive in leads I, aVF and the chest leads. The atrial depolarisation is complete in o. I
sec and the P wave should therefore not exceed 2i small squares in width. No electrical activity is
recorded as the impulse travels through the AV node to the Purkinje fibres. The QRS deflection
of the ventricular depolarisation should not start until 0.12 seconds after the start of the P wave
and not later than 0.2 seconds after it.
The effective initial direction of activation in the ventricle is dominated by activation of the
septum from the left side to the right. Other electrical forces in the right ventricle and the free
wall of the left ventricle cancel each other out. This activation wave moves downwards, to the
right, and anteriorly . Therefore usually there is a small initial Q wave in I, V6 and an R
wave in Vi. After septal activation, the dominant contribution to the depolarization wave arises
in the free wall of the left ventricle arrow . The force is downwards to the left and posteriorly.
Therefore, usually there is an R wave in I, aVF, V6 and a deep S in Vi. Ventricular activation is
complete within o.io seconds and the width of the QRS complex should not exceed 2k small
squares. The ventricular repolarisation wave roughly follows that of depolarisation, but moves
more anteriorly. Therefore, the T wave in leads I, aVF and V6 is similar in positivity to the QRS
complex, but it may be positive in the anterior chest leads where the dominant QRS is negative.
The time interval from the beginning of the QRS complex to the end of the T depends on heart
rate but is usually not more than 0.42 seconds (io ￡ small squares). If the T wave becomes
abnormal its direction is generally away from the anatomical site of abnormality.

INTERPRETATION OF THE ABNORMAL ECG

1. Since the P wave represents atrial activity and the QRSventricular activity the
electrocardiogram can be used to determine heart rhythm.
2. Damage to the conducting tissue will alter the pathways of activation and may alter the
QRS morphology.
3. Increased muscle mass will alter the amplitude and duration of P and QRS waves and
this allows recognition of hypertrophy of the muscle in different chambers of the heart.
4. Loss of muscle mass alters the QRS and allows recognition of myocardial infarction.
5. Many factors can alter the patterns of repolarisation and these can be suspected from
changes in the ST-segment and T waves.
Arrhythmias
ECTOPIC BEATS
A beat arising from a focus in the ventricle occurs prematurely. Since its activation route does
not initially involve the specialized conducting tissues the complex is wide and of a different
shape to the sinus beat. Since it makes the ventricle refractory to the following sinus beat the
next conducted sinus beat occurs after a ‘compensatory pause’.
A supraventricular ectopic beat (arising in the atria or in the atrioventricular node) is also
premature but generally has the same QRS morphology as the sinus beat, and the following
pause is less long.

TACHYCARDIAS
A rapid series of beats - ventricular or supraventricular - produces paroxysmal or sustained
tachycardia. This can be dangerous as cardiac function is less efficient and the oxygen and
metabolic needs of the heart are increased. The QRS complexes are wide and different in shape
to the sinus
beats. The end of die paroxysm is followed by the ‘compensatory pause’.

VENTRICULAR FIBRILLATION
Ventricular fibrillation occurs with completely chaotic electrical activity in the heart. No
coherent contraction occurs and this is the commonest cause of cardiac arrest. The tracing shown
was taken from a man in the early phase of acute myocardial infarction in 1972. Sinus rhythm
was obtained by electric shock. He survived this incident and remains well. Ventricular
fibrillation may occur without warning, follow a ventricular ectopic beat, especially if it is very
premature, or degenerate from ventricular tachycardia.
ATRIAL FIBRILLATION
Atrial fibrillation occurs with chaotic electrical activity of the atrial muscle with no coherent
atrial contraction. The P wave disappears and the base line shows irregular deflections.
Refractory cells in the atrioventricular node prevent very rapid stimulation of the ventricle. The
ventricle response is irregular.
Chamber hypertrophy
In left atrial hypertrophy the P wave is wide and in right atrial hypertrophy the P wave is tall. In
left ventricular hypertrophy the free wall of the left ventricle is thickened and the R wave in
leads looking to the left (I, V6) and the S wave in leads looking to the front are increased. The
tall R can be seen in a patient with mitral regurgitation. When left ventricular hypertrophy
increases in severity there is also an abnormality in repolarisation giving ST
depression, T wave inversion, the repolarisation wave moving away
from the left. In right ventricular hypertrophy the normally thin right ventricle is thick and
contributes forces to the QRS moving towards the right and anteriorly. This shows as an S wave
in I and an R wave in Vi. There is some similarity between this and right bundle branch block,
but in right ventricular hypertrophy the QRS is not abnormally prolonged.
Myocardial infarction
The first ECG evidence of acute myocardial infarction is marked
elevation of the ST-segment - the electrical forces moving towards
the direction of the site of infarct . This is followed typically with the loss of electrical forces in
the direction of the site of the infarct and T wave forces moving away from the infarct. In:
anterior infarction there is a loss of R wave in V1-4 giving \ a QS pattern in leads V1-3 with T
wave inversion.
In inferior infarction, the loss of the R waves is in the leads looking at the inferior surface of the
heart, i.e. II, III and aVF. There is ST-segment elevation in the same leads and T wave inversion
has appeared in lead 3. ST-segment depression is also present in leads I, and aVF. This so-called
reciprocal depression generally means a more extensive infarction.
REFERENCES
Echocardiography
 Hampton, J. R. (1980). The Electrocardiogram Made Easy, 2nd edition.Churchill
Livingstone, Edinburgh.
 Patricia A. Downie Fcsp. Cash’s Textbook of Chest, Heart and Vascular Disorders for
Physiotherapists 4TH edition, page no. 163-169.
Stress testing
 Acampa W, Assante R, The role of treadmill exercise testing in women. 2016;Oct;23(5)
991-996.
 William D. McArdle, Frank I Katch, Victor L. Katch. Exercise physiology: energy,
nutrition, and human performance., sixth edition.