A Guide to the Physical Examination - By Dr. Sam Gharbi

Guide to the
Physical
Examination
Understanding Medicine
Written by
Sam Gharbi
MD, CM, FRCPC
Contributions by
Iain Mackie
MD, FRCPC

i
Guide to the
Physical
Examination
Preface

DISCLAIMER
ii
Disclaimer
Extensive effort has been exerted in order to make this book as accurate as possible.
However, the accuracy and completeness of the information provided cannot be guaran-
teed. This book is to be used as an educational guide only, and healthcare profession-
als should use sound clinical judgement and individualize therapy to each specific pa-
tient care situation.
The author makes no claims whatsoever, expressed or implied, about the authenticity,
accuracy, reliability, completeness, or timeliness of the material presented in this book.
In no event shall the author be liable to any party for indirect, direct, special, inciden-
tal, or consequential damages, including but not limited to lost profits arising out of the
use of this book, even if the author has been advised of such damage.
By having read the above, or by use of this book, be it partially or in its entirety, you
have explicitly consented your agreement to the above disclaimer.

COPYRIGHT
iii
© Copyright Sam Gharbi 2013. All Rights Reserved

To Iain Mackie, for all his years of mentoring & friendship.
This book would not have been possible without his support.
DEDICATION
iv

I had always envisioned a better model for learning than the
traditional textbook, particularly in the 21st Century. This
guide is meant to combine the written word with pictures,
videos, as well as dynamic e-tools for note taking, highlight-
ing, study cards and other memory aides in an effort to cre-
ate an integrated environment that evolves with the learner
from day 1 of medical school until completion of training,
and hopefully beyond.
My sincere hope is that you will find it helpful this a useful
educational resource over the course of your medical train-
ing.
Good luck.
FOREWORD
v

VITALS & GENERAL
APPEARANCE
CHAPTER 1
6
Vitals
• Blood Pressure
• Heart Rate
• Respiratory Rate
• Oxygen Saturation
• Temperature
General
Appearance
• Stable vs Distress
• Pallor
• Cyanosis
• Diaphoresis
• Cachectic
Remember to always begin your physical examination
of patients with a set of full vital signs.

Definitions
• Note that some sources also identify pre-hypertension as a systolic BP be-
tween 120 & 140 and the diastolic BP >80.
• Note that there are slight differences between American, Canadian, & Euro-
pean guidelines in terms of the above classifications. I would recommend
reading the guidelines for further details on intricacies.
Blood Pressure Cuff Sizes
• Remember that you must always adjust the size of the blood pressure cuff used
in relation to the patient's size.
• The bladder of the BP cuff is the part of it that inflates with air. The width of
this bladder of the cuff should be roughly 40% of the upper arm circumference.
• The length of the bladder of the cuff should be roughly 80% of the upper arm
circumference.
BLOOD PRESSURE
SECTION 1
7
Physical Examination
SYSTOLIC DIASTOLIC
Normal <140 <90
Hypotension <100 <60
Hypertension >140 >90
Hypertensive urgency >180 >110
Hypertensive emergency
Any elevated BP at which there are
signs of end organ damage
Any elevated BP at which there are
signs of end organ damage

• If the blood pressure cuff is too small for your patient, then the BP reading ob-
tained will be higher than its actual value.
• Conversely, if the BP cuff used is too big for your patient, then the BP reading
obtained will be lower than its actual value.
Blood Pressure Measurement
1. No smoking, nicotine, or caffeine 1 hour prior to measurement of BP.
2. The patient should be resting for at least 5 minutes prior to BP measurement.
3. Have the patient sit, legs uncrossed, feet touching the ground. The patient
should be refrained from talking during the BP measurement.
4. Have the patient uncover their arm of any clothing, then extend the arm up to
the level of their heart (or mid-chest), with their palm facing upward and the pa-
tient's arm supported by yours.
5. Ensure that the center of the blood pressure cuff is over the brachial artery.
6. Place the diaphragm of the stethoscope directly over the brachial artery.
7. Raise the cuff pressure by inflating it as rapidly as possible to 140 mm Hg and lis-
ten for Korotkoff sounds. If they are present, pump the cuff another 20 mm Hg.
Continue auscultating and pumping the BP cuff as described until no Korotkoff
sounds are heard.
8. Once no Korotkoff sounds are heard, slowly deflate the cuff at a rate of about 5
mm Hg per per second until the first Korotkoff sounds of the systolic blood pres-
sure are heard. Record it as this is your patient's systolic blood pressure.
9. Continue to deflate the cuff at the above mentioned rate until no Korotkoff
sounds are heard. This is the diastolic pressure.
10. Whenever you are measuring the blood pressure, you should also consider ex
amining for Pulse Pressure & Pulsus Paradoxus (See Chapter 2)
8
Physical ExaminationPhysical Examination

Definitions
• A normal heart rate is between 60 beats per minute (bpm) and 100 bpm.
• A heart rate less than 60 bpm is low, and defined as bradycardia.
• A heart rate greater than 100 bpm is high, and defined as tachycardia.
HEART RATE
Normal between 60 & 100 bpm
Low <60 bpm
Elevated >100 bpm
Measurement
• The heart rate is typically measured by palpating the patient's radial artery and
counting the number of beats felt over 60 seconds (or alternatively over 15 sec-
onds and multiplying that number by 4 to give you the heart rate in beats per
minute).
• Alternatively, the heart rate can also be measured electronically with monitors
and other tools.
• Remember to always record not just the rate, but also the rhythm whenever feel-
ing a pulse. Particularly, note whether the rhythm is regular or irregular. Irregu-
lar rhythms may be indicative of underlying pathological cardiac rhythms. One
of the most common irregular rhythms is Atrial Fibrillation, which manifests as
an irregularly irregular rhythm. (see Chapter 2 for more on pulses)
HEART RATE
SECTION 2
9

Clinical Correlate
• Bradycardia can be life threatening, mainly because it causes too little pumping of
the heart and hence hypoperfusion of organs. This can be caused by a myriad of pa-
thologies, the most common of which are often a history of myocardial infarct or
drug toxicity. The most common complaints in patients with bradycadia are weak-
ness, lightheadedness/pre-syncope, and/or syncope.
• Tachycardia needs to be determined whether it is sinus tachycardia, or a tachyar-
rhythmia. In other words, whenever you have a patient with an elevated heart rate,
you must determine whether that tachycardia is of a normal rhythm that is inherent
to the heart (ie. sinus) or whether it is an abnormal rhythm (arrhythmia). This is
done by getting a 12 lead ECG.
• Sinus tachycardia can be caused by such elements as stress, anxiety, pain, & caffeine
for example. Tachyarrhythmias can be caused by a myriad of pathologies, including
myocardial infarct, drugs, and metabolic abnormalities. Patients with tachycardia
often complain of palpitations, as well as potentially experiencing chest pain, dysp-
nea, pre-syncope, and/or syncope.
10

Definitions
• The normal range for the respiratory rate runs between 12 and 20 breaths per minute.
• An elevated respiratory rate is referred to as tachypnea, and is defined as anything
equal or greater than 20 breaths per minute.
Measurement
• The respiratory rate is often measured by simply observing the patient breathing and
counting the number of breaths over a minute span.
• Remember that if you mention to your patient that you are counting the number of
their breaths, they will often get self-conscious of their breathing, which may poten-
tially bias your measured result. One tip that physicians use is to continue palpating
the pulse, as part of the evaluation of the heart rate (see previous section), while in
fact observing the patient's breathing over 15 seconds and averaging that out over a
minute.
Clinical Correlate
• Patients with a low respiratory rate are not oxygenating adequately, which may ulti-
mately be life threatening as they are not providing enough oxygen into the blood to
the tissues. Common causes of this can be stroke, spinal chord injury, as well as
drugs & toxins.
• Patients with an elevated respiratory rate are often compensating for a lack of oxygen.
Causes vary from primary lung pathologies, infections, metabolic abnormalities, and
drugs & toxins.
RESPIRATORY RATE
SECTION 3
11

Definitions
• The normal range for human body temperature usually is defined as being any-
where between 35 and 37.9 degrees Celsius.
• An elevated temperature (measured orally), referred to as a fever, is defined as
any temperature greater than 38 degrees Celsius.
• A low temperature (measured orally), referred to as hypothermia, is defined as
any temperature less than 35 degrees Celsius
Measurement
• The temperature of a patient can be taken with a thermometer either orally,
rectally, or axillary.
• Note that rectal temperatures are often higher than oral temperatures by an av-
erage of 0.5 degrees Celsius, while axillary temperatures are often lower than
oral temperatures by an average of 1 degree Celsius.
• In adult patients, it is generally recommended to measure the temperature
orally. Axillary temperatures are considered the least accurate of the 3 above
options.
TEMPERATURE
SECTION 4
12
TEMPERATURE (CELSIUS)
Normal 35 to 37.9 degrees
Low <35 degrees
High >38 degrees

Clinical Correlate
• Fever often hints at possible underlying infection, but also can be seen with
most any inflammatory disorders, malignancies, or certain drug intoxications
and/or side effects.
• The differential diagnosis for fever is quite broad, but particular attention
should always be paid to investigating and ruling out any possible infectious
process in a patient with an acute spike in temperature.
• Note that when taking a history, patients may state that they had a fever at
home, but remember to always ask whether they actually took their tempera-
ture with a thermometer. Many patients state that they were febrile but are in
fact eluding to a subjective sense of warmth rather than actually having quanti-
fied their temperature.
13

Definitions
• A normal blood oxygen saturation range is between 92% to 99%.
Note that it is not technically possible to have 100% oxygen saturation while
breathing room air.
Measurement
• The blood oxygen saturation is measured using a blood oxygen saturation
probe, or commonly referred to as a "sat probe", which is usually put on one
of the patient's fingers and provides a measurement of the level of blood oxy-
gen saturation.
Clinical Correlate
• Any blood oxygen saturation less than 92% is considered abnormal & can re-
sult in tissue hypoperfusion. If severe enough, it can result in respiratory ar-
rest & death.
• The one major exception for the above blood oxygen saturation cutoff is in pa-
tients with Chronic Obstructive Pulmonary Disease (COPD), where a value
greater than 88% is considered appropriate and not necessarily a sign of
acute respiratory compromise. In fact, many patients with COPD are often
recommended to be kept at an oxygen saturation between 88 and 92% (refer
to readings on COPD for further explanations regarding pathophysiology).
OXYGEN SATURATION
SECTION 5
14

Definitions
• The term pulse pressure is actually somewhat fo a misnomer. It actually does not have
to do with measurement of the pulse, but instead it has to do with the blood pressure.
• The Pulse Pressure is defined as the systolic pressure minus the diastolic pressure:
Pulse Pressure = Systolic BP – Diastolic BP
• The normal range for the pulse pressure at rest is no greater than 40 mm Hg, although
according to some sources 60 mm Hg is the upper extreme of normal.
Interpretation
PULSE PRESSURE
SECTION 6
15
Pulse PressurePulse Pressure
Pulse Pressure
< 25 mm Hg
• Shock
• Cardiac Tamponade
• Congestive Heart Failure
• Aortic Stenosis
Pulse Pressure
> 60 – 80 mm Hg
• Aortic Regurgitation
• Arterio-venous malformation (AVM)
• Hyperthyroidism

Definitions
• An abnormal Pulsus Paradoxus is a decrease in systolic pressure during inspiration
>10 mm Hg
• In healthy individuals, the Pulsus Paradoxus should not be greater than 10 mm Hg.
Some sources note a value <15 mm Hg as being the upper limit of normal.
• The term Pulsus Paradoxus is a misnomer in 2 senses. Firstly, it is not a pulse, but a
medical sign noted upon examination of the blood pressure. Secondly, there is noth-
ing paradoxical about Pulsus Paradoxus, it is simply an exaggeration of a normal phe-
nomenon.
Pathophysiology
• Why does Pulsus paradoxus occur? In fact, there are 3 different explanations:
1. Due to septal deviation into the left ventricular outflow tract upon inspiration.
2. Systolic pressure normally decreases during inspiration because lung capacity in-
creases with inspiration and the vascular bed expands. Therefore, less blood flows
from the lungs into the heart.
3. Intrathoracic pressure decreases with inspiration, and because the aorta is an intratho-
racic organ, its pressure also drops.
Measurement
1. Upon blood pressure examination, pump the BP cuff until you hear no Korotkoff
sounds
2. Slowly deflate the cuff, at a rate of roughly 1 mm Hg per second until you hear
Korotkoff sounds
PULSUS PARADOXUS
SECTION 7
16

3. Initially, Korotkoff's sounds will be heard only during expiration
4. Continue slowly deflating the BP cuff
5. At some point during cuff deflation, Korotkoff's sounds will be heard during inspira-
tion as well. The blood pressure difference between the two events will determine the
pulsus paradoxus.
6. Normally, in a healthy person, there is a decrease in systolic pressure during inspira-
tion no greater than 10 mm Hg. Anything greater than this value is considered an ele-
vated pulsus paradoxus and is potentially due to underlying pathology.
Clinical Relevance
• An increased pulsus paradoxus is characteristic of pericardial tamponade.
• It can also been seen in a number of various other conditions, such as in asthma exac-
erbations.
17

Overview
Whenever performing a physical examination, you must always comment on the pa-
tient's general appearance. However, often we unfortunately only use vague and sub-
jective terminology such as "the patient looks well" or "the patient appears stable".
These terms lend themselves to variable interpretation, and needless to say a staff per-
son with 30 years experience and a student with 30 days experience can have a very
different definition of a "stable" or "well looking" patient.
Although it is not necessarily wrong to use terminology such as "stable looking" in
your assessment of patients' general appearance, it is also critical that you provide fur-
ther quantifiable information in your report regarding the general appearance.
The following variables should routinely be reported in your assessment of the pa-
tient's general appearance:
General Appearance
• Pallor?
• Cyanosis?
• Jaundice?
• Diaphoresis?
• Cachectic?
• Accessory Muscle Use?
GENERAL APPERANCE
SECTION 8
18

Clinical Correlate
• Pallor - Pallor in itself is somewhat of a subjective quantification. Patients with
severe anemia may often appear pale.
• Cyanosis - Either central (tongue & lips) or peripheral (hands/digits), cyanosis
is quantified as a bluish tinge to the skin commonly due to low levels of oxygen
in the blood.
• Jaundice - This is defined as a yellow tinge to the skin in general, and is most
commonly due to underlying liver disease (ie. cirrhosis).
• Diaphoresis - This is defined as the patient appearing generally sweaty, and
can be associated with a patient having a myocardial infarct.
• Cachectic - Patients have muscle wasting and loss of subcutaneous fat are often
referred to as appearing cachectic. This can be due to malnourishment or malig-
nancy.
• Accessory Muscle Use - These muscles are the sternocleidomastoids, the sca-
lenes muscles, and the intercostals. Look for pronounced activity in these mus-
cle groups, as it suggests the patient is in respiratory distress and possible im-
pending respiratory failure. Another associated sign of respiratory distress & fail-
ure on general inspection is paradoxical abdominal breathing, where the abdo-
men moves in with inspiration, not out as it usually should.
19

CARDIAC EXAM
CHAPTER 2
20
• Jugular Venous Pressure (JVP)
• Carotid & Peripheral PulsesPulses
Inspection
• Congenital Malformations
• Scars
• Pacemaker
Palpation
Auscultation
• Heaves
• Thrills
• Apex Beat
1. Heart Sounds:
- Normal Heart Sounds
- Loud or Soft S1 and/or S2
- Extra Heart Sounds (S3 & S4)
2. Heart Sound Splitting:
- Physiological Splitting of S2
- Paradoxical Splitting of S2
- Wide Splitting of S2
- Fixed Splitting of S2
3. Murmurs:
- Timing (systolic vs diastolic)
- Shape (early/mid/late/holo)
- Grade (I to VI)
- Location (RUSB/LUSB/Apex)
- Radiation (Carotids/Apex/Axilla)
- Maneuvers
4. Pericardial Rubs
Overview

Physiology
•The jugular venous pressure (JVP) reflects changes in pressure within the right atrium
of the heart.
•If the JVP is low, then it generally reflects a state of hypovolemia.
•Elevated jugular venous pressure (JVP) is also sometimes referred to as jugular venous
distension (JVD), and can be as a result of hypervolemia or a multitude of other etiolo-
gies, including:
Causes for an Elevated JVP
Congestive Heart Failure/Right Heart Failure
Tricuspid Stenosis or Regurgitation
Pericardial Tamponade
Constrictive Pericarditis
•In terms of etiologies for an elevated JVP, one of the major causes is congestive heart
failure (CHF), or more specifically right heart failure. In CHF, the heart is incapable of
effectively pumping blood to the tissues, hence there is an increased volume load on the
heart which causes congestion and backflow up the jugular veins, resulting in an ele-
vated JVP.
•In tricuspid valve pathology, an elevated JVP can result from either stenosis or regurgita-
tion of the valve, which produces increased backflow up the jugular veins.
•In constrictive pericarditis, the heart contractility is diminished,and hence there is an in-
creased volume load in the heart causing an increased JVP.
JUGULAR VENOUS PRESSURE (JVP)
SECTION 1
21

Components of the JVP:
• There are various components at a physiologic level to the JVP. Variations in each of
these components can be clues to underlying pathology.
“a” Wave:
• The “a” wave is prior to ventricular systole (meaning it occurs before S1).
• The “a” wave is produced by venous distension from right atrial contraction.
• The “a” wave is absent in patients with atrial fibrillation since there is ineffective ven-
tricular filling from the right atrium due to impaired atrial contraction.
• Large “a” waves (called “cannon a waves”) indicate that the right atrium is contracting
against increased resistance. Cannon “a” waves are indicative of underlying pathol-
ogy, such as ventricular tachycardia or 3rd degree block (where the right atrium is con-
tracting against a closed tricuspid valve).
Causes for Canon "A" Waves
3rd degree heart block
Ventricular Tachycardia
22
JVP Components

“v” Wave:
• The “v” wave occurs at the same time as S2.
• This late systolic “v” wave results from the right atrium reaching its maximal filling
point at the end of systole (keeping in mind that the tricuspid valve is closed during
systole).
Causes for Prominent "v" Waves
Tricuspid Regurgitation
Severe CHF exacerbation
“c-v” Wave:
• The “c-v” wave is a pathologic wave. It is a distinct monophasic JVP wave instead
of the usual biphasic wave of the JVP.
• The monophasic “c-v” wave occurs when the “c” notch is more prominent and ends
up fusing with the “v” wave, hence the monophasic JVP appearance.
• The “c-v” wave is distinctly seen in Tricuspid Regurgitation.
Causes for "c-v" Waves
Tricuspid Regurgitation
23

Summary of Pathologic JVP Wave Forms
Wave Form Differential Diagnosis
Canon a wave • 3rd degree heart block
• Ventricular Tachycardia
Prominent a wave • Pulmonary Hypertension
• Tricuspid Stenosis
Absent a wave • Atrial Fibrillation
c-v wave • Tricuspid Regurgitation
Prominent v wave • Tricuspid Regurgitation
• Severe CHF exacerbation
Monophasic JVP • Atrial Fibrillation
• Tricuspid Regurgitation
24

Examination of the JVP
1. Patient must be at an angle, usually starting at 45°, with their head
tilted upwards and facing slightly away from you.
2. It is commonly taught that it is preferable to use the internal jugular
over the the external jugular. The external jugular is lateral to sterno-
cleidomastoid (SCM) and easier to see. Internal jugular is medial and
sometimes behind the clavicular head of SCM, hence it is more diffi-
cult to see.
3. Start at the top of the path of the internal jugular vein, and work your
way downwards looking for a biphasic pulsation. As soon as you this,
stop. This is the JVP.
4. Once you find the JVP, use a ruler to measure its vertical height to the
sternal notch. This measured height is the value for the JVP. Note
that most experienced staff simply eyeball this value rather than using
a ruler.
25
Internal Jugular Vein Path
External Jugular Vein Path

5. A height >3cm above the sternal angle is considered an elevated value.
An easy way to remember this value of >3 cm as a cutoff is that JVP
has 3 letters.
6. To get an estimate of the right atrial pressure (or central venous pres-
sure) from the JVP, add 5cm to the observed value of the JVP height
above the sternal angle. This value will give you a pressure in cm
H2O. However, since mm Hg are the standard units in which the right
atrial pressure (or CVP) is measured, you will need to convert it into
mm Hg by multiplying it by 1.5 to estimate the right atrial pressure.
26

JVP Characteristics
Summary of JVP Characteristics
1. Multiphasic
2. Non-palpable
3. Occludable
4. Decreases with sitting up
5. Decreases with inspiration
6. Abdomino-jugular reflux
1) Biphasic
• There are 2 pulsations in the JVP for each contraction of the heart, while the carotid
artery only has one pulsation observed for each cardiac cycle.
2) Non-palpable
• The JVP cannot be palpated. If one feels a pulse in the neck, it is generally from the
carotid artery.
3) Occludable
• The jugular venous pulsation can be extinguished by occluding the internal jugular
vein by pressing lightly at the base of the neck.
4) Varies with posture
• The JVP varies with the angle of the neck, where it decreases the more the patient is
sitting up vertically. Essentially, when a person is standing or sitting up, the JVP
will appear lower, while when they are supine it will appear higher. The carotid
pulse does not vary with position.
5) Varies with inspiration
• The JVP usually decreases with deep inspiration. This is a consequence of the
Frank-Starling mechanism, as inspiration decreases the thoracic pressure and in-
creases blood movement into the heart (ie. Venous return increases).
27

6) Abdomino-Jugular Reflux (AJR)
Definition:
• Also known as Hepatojugular reflux or Abdominal Compression Test.
• Abdominal compression increases venous return and pressure, as a result facilitating
analysis of the jugular venous pulse.
Phyisology:
• Overall, the mechanism for hepato-jugular reflux has not been clearly elucidated. It
is assumed that a failing right ventricle is unable to respond normally to the in-
creased preload caused by increased venous return with abdominal compression and
elevated intra-abdominal pressure.
• In addition, a raised diaphragm during abdominal compression compromises cardiac
filling by decreasing the intrathoracic and mediastinal volumes available for cardiac
expansion.
• Thus, abnormal elevation of systemic venous pressure may be the consequence of
volume expansion and a raised diaphragm during abdominal compression.
Method:
1. Begin by exerting anywhere between 15 and 30 mm Hg of pressure (can use a blood
pressure cuff) over the abdomen with the fingers spread. More pressure can be ap-
plied in this manner without producing discomfort. The pressure does not necessar-
ily need to be on the right upper quadrant.
2. Apply abdominal pressure for 15 to 30 seconds.
3. The JVP will transiently rise by at least 1 cm to 3 cm in a healthy patient. This in-
crease is not sustained, meaning it lasts less than 3 cardiac cycles. According to cer-
tain sources however, there is no increase in JVP with abdominal compression in pa-
tients who are not volume overloaded. Regardless of the volume status however,
the carotid pulse will remain unaffected by this maneuver under any circumstance.
4. In patients with volume overload however, there is sustained elevation of venous
pressure greater 3 cm during continued compression.
28

29
Video Overview of JVP
Video Overview of AJR

Definition:
• Kussmaul's sign is defined as either no change or an increase in the JVP during inspi-
ration.
• This is in opposition to the fact that the JVP should normally decrease with inspira-
tion
Pathophysiology:
• The mechanism of Kussmaul's sign is not entirely clear. Increased resistance to right
atrial filling during inspiration appears to be a contributory factor.
Etiology:
Causes
Classically • Constrictive pericarditis
Less commonly • Pericardial tamponade
• Massive pulmonary embolism
• Right ventricular infarction
• Restrictive cardiomyopathy
30
Kussmaul’s Sign

When taking a patient's pulse, you should note the patient's pulse rate, the strength of the pulse, and
the regularity of the pulse.
1) Pulse Rate:
Pulse Rates
Normal = 60 to 100 bpm
Tachycardia = heart rate >100 bpm
Bradycardia = heart rate <60 bpm
2) Strength:
• The strength (force) of the pulse is determined by the amount of blood forced into the artery by
the heartbeat.
• Note that there is much inter-observer variability when it comes to defining the pulse strength,
and that its clinical significance is limited.
• The strength of the pulse can be defined as:
Pulse Types & DefinitionsPulse Types & Definitions
Bounding If the heart is pumping a large amount of blood with
each heartbeat, the pulse will feel very strong. This
strong pulse is called "bounding" pulse.
Strong A strong pulse is stronger than normal pulse, but is
less than bounding.
Normal Normal
PERIPHERAL PULSES
SECTION 2
31

3) Rhythm:
• Regular
• Regularly Irregular
• Irregularly Irregular
4) Pathological Pulses:
• Irregularly irregular pulse
• Pulsus Bisferiens
• Pulsus Alternans
• Pulsus Parvus e Tardus
32
Irregularly Irregular Pulse
Pulsus Paradoxus
Irregularly Irregular PulseIrregularly Irregular Pulse
Definition • Irregularly irregular pulse
Method of detection • Palpate radial artery
Associated pathology • Atrial Fibrillation
Pulsus ParadoxusPulsus Paradoxus
Definition • This is a misnomer, as it is not a pulse
but a finding on blood pressure
measurement. Please refer to section
on blood pressure for further
information.

33
Pulsus Bisferiens
Pulsus BisferiensPulsus Bisferiens
Definition • It is a twice beating pulse
• It has 2 systolic peaks due to a midsystolic
dip.
Pathophysiology • The mechanism of pulsus bisferiens is not
clear. It is believed to be associated with
the rapid ejection of a large volume of
blood during systole through the aortic
valve.
Location for palpation • Carotid or Radial Artery
Method of detection • Palpate the radial artery and feel for a twice
beating pulse.
Associated pathology • Hypertrophic Cardiomyopathy
• Severe Aortic Regurgitation
• Can also be observed in patients who have a
combination of severe Aortic Regurgitation
with moderate Aortic Stenosis.

34
Pulsus Alternans
Pulsus AlternansPulsus Alternans
Definition • Defined as a regular alteration of pulse amplitude
between strong and weak
Pathophysiology • It is due to alternating left ventricular contractile force,
and usually indicates severe impairment of left
ventricular function
Location for palpation • More marked as the pulse moves peripherally, hence
best detected in the radial arteries.
Method of detection • Use 2 fingers to apply light pressure to the radial artery;
by increasing the pressure with the proximal finger, the
weaker beats can be eliminated under the distal finger.
• Pulsus alternans should not be diagnosed when the
cardiac rhythm is irregular.
Associated pathology • Congestive Heart Failure (LV dysfunction)

35
Pulsus Parvus e Tardus
Pulsus Parvus e TardusPulsus Parvus e Tardus
Definition • Defined as a weak & slow pulse
Pathophysiology • It results from obstruction of the left ventricular outflow
tract.
Location for palpation • Carotid artery and Apex of the heart concomitantly need
to be palpated for a delayed carotid upstroke in relation
to the apex beat.
Method of detection • Can usually only feel it when there is a narrow pulse
pressure (<25 mm Hg)
Associated pathology • Aortic Stenosis

Overview
When performing a full cardiac exam, you must generally inspect for the following:
Scars
Usually midline, indicative of previous cardiac surgeries (ie. CABG)
Pacemaker
Usually located subcutaneously within the upper thoracic areas. There will often
be a scar in this area as well from the initial pacemaker insertion.
Congenital Malformations
Pectus excavatum - can be associtated with mitral valve prolapse
Pectus carinatum - purely cosmetic
INSPECTION
SECTION 3
36
Look for CABG scars here, as well as
pectus excavatum & carinatum here
Look for pacemaker here

Overview
When performing a full cardiac exam, you must always perform palpation
after inspection. On palpation, you must look for:
1. Cardiac Heaves
2. Cardiac Thrills
3. Apex Beat
Note that there is no percussion component to the routine & full cardiac ex-
amination.
PALPATION
SECTION 4
37

Cardiac Heaves
Examination:
• For parasternal heaves, use the proximal portion of your palm to palpate the left side of the ster-
num for any sustained outward motion (ie. heave).
• For subxiphoid heaves, use the tip of ur fingers placed below the xiphoid process to feel for the
heart border.
Clinical Relevance:
• A cardiac (or parasternal) heave is indicative of underlying right ventricular hypertrophy or left
atrial hypertrophy. In order to distinguish between the 2:
• Right ventricular hypertrophy =
Parasternal + Subxiphoid heave, both of which synchronous with apex beat
• Left atrial hypertrophy =
Parasternal heave, not synchronous with apex beat
38
Video Overview of Cardiac Heave Exam

Cardiac Thrills
Definition:
• The definition of a thrill is palpable turbulence. Thrills are vibratory sensations from turbulent
blood flow across valves of the heart.
Examination:
• When examining for thrills, palpate the same 4 areas that you would auscultate.
• The proper technique of palpation for a thrill is to place the joints at the base of the fingers onto
the chest at each of the areas mentioned above. The base of the fingers are used because they
are more sensitive to vibration sensation than the tip of the fingers.
• When palpating for thrill, apply gentle pressure, because if too much pressure is applied the
thrills will not be felt.
Clinical Relevance:
• Thrills are indicative of underlying valvular pathology. Essentially, a thrill is palpable turbu-
lence. The presence of a thrill indicates an underlying murmur.
• Thrills are associated with a Grade IV cardiac murmur, however are not necessarily associated
with Grades V or VI.
39
Video Overview of Cardiac Thrill Exam

Apex Beat:
• The apex beat usually corresponds to the left ventricular apex of the heart, however it can also
correspond to the right ventricle in patients where there is significant right ventricular hypertro-
phy.
• The term point of maximal impulse (PMI) is often used as a synonym for an apex beat, how-
ever this is not accurate. The term PMI should be avoided because the maximum precordial
pulsations may be due to such abnormalities such as a large right ventricle, dilated pulmonary
artery, a ventricular aneurysm, or an aortic aneurysm.
Examination:
• The apex beat is most easily detected with the patient in a sitting position.
• To detect the apex beat, your fingertips should be applied to the chest in the 5th intercostal
space at the midclavicular line, or alternatively 10 cm from the midsternal line. The apex beat
should be the most laterally palpated impulse located in this region.
• Alternatively, to detect the apex beat, some would recommend to begin with your fingertips at
the mid-axillary line at the 5th intercostal space and move medially (towards the sternum) until
you feel the apex beat.
• A normal apex beat should be no larger than 3cm in diameter.
• If the apex beat cannot be felt with the patient sitting, the patient should be re-evaluated in the
supine and left lateral decubitus positions. Understand however that in the latter position, the
apex beat can be displaced slightly to the left even in healthy individuals.
40
Apex Beat

Clinical Relevance:
• A sustained apex beat is defined as being 2/3 the duration of systole, and indicates concentric
left ventricular hypertrophy (LVH).
• A displaced apex beat is defined as either an apex beat located lateral to the midclavicular line,
or alternatively past 10 cm from the midsternal line. A displaced apex beat is indicative of ec-
centric LVH and dilatation of the left ventricle.’
• Note that a patient can have both a sustained apex beat as well as a displaced apex beat.
41
Video Overview of Apex Beat Exam

Overview
In cardiac auscultation, you must auscultate at 4 different positions in the chest. Each position repre-
sents sound emitted from a particular valve of the heart. At each position, you must listen for:
1. Quality of normal hearts sounds S1 and S2 and presence of any splitting
2. Presence of any abnormal heart sounds (gallops) S3 & S4
3. Presence of any murmurs
AUSCULTATION
SECTION 5
42
Video Overview of Cardiac Auscultation

Normal Heart Sounds
S1 - First Heart Sound:
• The first heart sound, S1, indicates the beginning of systole
• It is caused by the sudden block of reverse blood flow due to closure of the mitral and tricuspid
valves at the beginning of ventricular contraction (ie. the beginning of systole)
S2 - Second Heart Sound:
• The second heart sound, S2, indicates the end of systole/beginning of diastole
• It is caused by the sudden block of reversing blood flow due to closure of the aortic valve and
pulmonary valve at the end of systole (ie. the beginning of diastole)
• S2 is composed of 2 components, A2 (which represents aortic valve closure) and P2 (which rep-
resents pulmonic valve closure). They can be heard during inspiration, where there is physiol-
ogic splitting of S2.
P2 - Pulmonic Component of S2:
• Prominent P2 is heard in pulmonary hypertension, and is usually present when there is splitting
of S2 heard when auscultating past the 4th intercostal space. You should not routinely hear split-
ting of S2 past the 4th intercostal space. If you do, then you are hearing a P2.
43

Heart Sound Splitting
Physiologic Splitting of S2:
 
• S2 splits into an Aortic (A2) and Pulmonic (P2) components during inspiration
• The A2 component represents the sound emitted from closure of the aortic valve. The P2 com-
ponent represents the sound emitted from the closure of the pulmonic valve. Both of these 2
components of the S2 can be heard during inspiration in auscultation of healthy patients.
• Physiologically, this phenomenon is due to the fact that with inspiration comes an augmented
inflow of blood into the right ventricle, which increases the right ventricle's stroke volume and
ejection period. As a result, this delays the closure of the pulmonic valve. Therefore the sound
from the pulmonic valve closure (P2) is heard slightly after the sound from aortic valve closure
(A2).
44

Paradoxical Splitting of S2
• In paradoxical splitting, there is a reversal of the normal closure sequence with pulmonic clo-
sure occurring before aortic closure
• In paradoxical splitting, the second sound is single during inspiration and splits instead during
expiration
• Paradoxical splitting is caused by either delayed depolarization of the left ventricle or pro-
longed left ventricular ejection time
• The paradoxical splitting of S2 may be heard in:
Causes for Paradoxical Splitting of S2:
• Left Bundle Branch Block (LBBB)
• Aortic Stenosis
• Aortic Regurgitation
• Myocardial Infarct
• Hypertrophic Obstructive Cardiomyopathy
45

Wide Splitting of S2
• The second heart sound (S2) can be widely split if there is an early A2 or a delayed P2. In
other words, there is a widely split S2 if there is a delayed closure of the pulmonic valve.
• Causes for a wide splitting of S2 include:
Causes for Wide Splitting of S2:
• Right Bundle Branch Block (RBBB)
• Pulmonary Stenosis
• Right Ventricular Heart Failure
46

Fixed Splitting of S2:
• This is when there is little or no change in the splitting of S2 between inspiration & expiration
• This happens in pathologies where the volume and duration of right ventricular ejection are not
significantly increased by inspiration, and hence there is minimal or no physiological splitting
of S2
• This is seen in usually in in Atrial Septal Defects (ASD)
47

Extra Heart Sounds (Gallops)
S3 - Third Heart Sound
• The third heart sound, S3, is a low pitched sound occurring after S2 during mid-diastole. The
S3 sound is actually produced in the ventricles.
• S3 is most commonly heard in conditions where there is left ventricular systolic dysfunction, or
in other words where there is a low ejection fraction. An S3 is also heard in conditions where
there is rapid ventricular filling.
Causes for S3:
• Poor Left Ventricular Function
- CHF/Cardiomyopathy
• Rapid Ventricular FIlling
- Severe Mitral Regurgitaiton
- Ventricular Septal Defect (VSD)
• Left-sided S3 is best heard at the apex of the heart with the bell of the stethoscope during expi-
ration and with the patient in the left-lateral position
• Right-sided S3 is best heard at the left lower sternal border and is usually louder with inspira-
tion
48

Extra Heart Sounds (Gallops)
S4 - Fourth Heart Sound:
• S4 is a low pitched sound heard during diastole before S1
• The sound is produced in the ventricle during diastole. Essentially, S4 occurs when there is a
diminished left ventricular compliance which increases the resistance to ventricular filling. An
S4 is therefore commonly heard in patients with left ventricular hypertrophy from any cause, or
in patients with myocardial ischemia
• S4 is frequently heard in patients with:
Causes for S4:
• Acute Myocardial Infarct
• Aortic Stenosis
• Hypertension
• Hypertrophic Cardiomyopathy
• S4 is best heard with the bell of the stethoscope.
• Both S3 and S4 may radiate to the carotids.
• S4 is absent in patients with atrial fibrillation.
49

Murmurs
• The opening and closing of the valves is usually much less loud than the sound of the blood
rushing through the valve and "colliding" with the subsequent barrier. Because of this, aus-
cultation to determine the function of a valve is usually not performed at the position of the
valve, but at a downstream position where the listener can best hear the blood colliding af-
ter the valve is closed. Hence, we listen at the following sites:
Valve Area of Auscultation
Aortic Valve (A) 2nd right sternal border
Pulmonary valve (P) 2nd left sternal border
Tricuspid valve (T) 4th left sternal border
Mitral valve (M) 5th left midclavicular line
50

Murmurs
Approach to describing a murmur:
1. Timing:
• Systolic
• Diastolic
2. Shape:
• Holosystolic
• Crescendo-descrescendo
• Early/Mid/Late peaking
3. Grade:
Cardiology – Physical Exam by Sam Gharbi
Approach to describing a murmur:
1. Timing:
• Systolic
• Diastolic
2. Shape:
• Holosystolic
• Crescendo-descrescendo
• Early/Mid/Late
3. Grade:
4. Location where best heard:
• 2nd
right parasternal
• 2nd
left parasternal
• 4th
left parasternal
• 5th
left midclavicular
5. Radiation:
• Apex
• Carotid arteries
• Axilla
6. Maneuvers
• Standing
• Squatting
• Valsalva
• Handgrip
Grading of Cardiac Murmurs
Grade 1 • Faintest murmur that can be heard
• Careful continuous auscultation in a quiet environment
Grade 2 • Moderately loud
Grade 3 • Loud without thrill
Grade 4 • Loud with thrill
Grade 5 • Very loud, with or without thrill
• Can be heard with the edge of the stethoscope
Grade 6 • Loudest, with or without thrill
• May be heard without a stethoscope/stethoscope off the chest
4. Location where best heard:
• 2nd right parasternal
• 2nd left parasternal
• 4th left parasternal
• 5th left midclavicular
5. Radiation:
• Apex
• Carotid arteries
• Axilla
6. Maneuvers
• Standing
• Squatting
• Valsalva
• Handgrip
51

Systolic Murmurs
Overview of Murmurs:
Systolic Murmurs
Aortic Stenosis:
• Crescendo-Decrescendo Murmur
• Best heard at left upper sternal
border (LUSB)
Severe Aortic Stenosis
• Late peaking murmur
• Soft or absent S2
• Best heard at LUSB
Mitral Regurgitation:
• Holosystolic Murmur
• Best heard at apex
Tricuspid Regurgitation:
• Holosystolic Murmur
• Best heard at the right or left mid
sternal border or at the subxiphoid
area
Mitral Valve Prolapse:
• Late Systolic Murmur
• Often preceded by a non-ejection
click
• Best heard at the apex
Non-Valvular Systolic Murmurs:
• Hypertrophic cardiomyopathy
• Ventricular septal defect
• Coarctation of the aorta
52

Diastolic Murmurs
Diastolic Murmurs
Aortic Regurgitation:
• Early diastolic mumur
• Best heard at the left upper sternal
border
Mitral Stenosis:
• Mid-diastolic murmur
• Often with an opening snap
• Best heard at the apex
Note: Continuous “Machinery” murmurs are most often indicative of PDA
53

Maneuvers in Auscultation
Use of Position in Cardiac AuscultationUse of Position in Cardiac Auscultation
Supine • General auscultation
Leaning forward and
holding expiration
• Aortic stenosis
• Aortic regurgitation
• Pericardial rubs
Left lateral decubitus Using the bell of the stethoscope:
• Mitral stenosis
• Gallops
Summary of Cardiac ManeuversSummary of Cardiac ManeuversSummary of Cardiac Maneuvers
Maneuver Increases the intensity of
the following murmurs
Decreases the intensity of
the following murmurs
Valsalva
&
Standing
• Hypertrophic
Cardiomyopathy
• Mitral Valve Prolapse
• Most other murmurs,
including AS, AI, MR
Squatting • Most murmurs • Hypertrophic
Cardiomyopathy
• Mitral Valve Prolapse
Handgrip • Most Murmurs
• Gallops
• Hypertrophic
Cardiomyopathy
54

Pericardial Friction Rub
• Friction rubs are heard because of an inflammation of the pericardial sac around the heart that
causes the parietal and visceral surfaces of the roughened pericardium to rub against each other.
This produces the friction rub sound, with both systolic and diastolic components.
• The sound resembles that of squeaky leather and is often described as grating, scratching, or rasp-
ing. The sound seems very close to the ear and may seem louder than or may even mask the other
heart sounds.
• Friction rubs are best heard when the patient is leaning forward, during expiration, between the
apex and sternum, but may also be widespread.
Friction Rub Heard Best When...
• Patient Leaning Forward
• Auscultating between apex and sternum
• During Expiration
• One, two, or three components of a pericardial friction rub may be audible. A three-component
rub indicates the presence of pericarditis and serves to distinguish a pericardial rub from a pleural
friction rub, which ordinarily has only two components.
• In a triphasic cardiac rub, the 3 components of that pericardial rub are sounds from:
o Diastole
o Atrial systole
o Ventricular systole
55

RESPIRATORY EXAM
CHAPTER 3
56
Overview
Auscultation
Percussion
Palpation
Inspection
• Cyanosis (peripheral & central)
• Accessory Muscle Use
• Paradoxical breathing
• Clubbing
• Chest excursion
• Tactile Fremitus
• Routine Percussion
• Air entry
• Wheeze
• Crackles

Note that when performing a complete physical exam on a patient, most of the in-
spection components of the respiratory exam will already have been performed
under the general appearance exam. However, in an exam situation where you
may be asked to demonstrate the respiratory examination, you should include the
below items on inspection:
Cyanosis
Either central (tongue & lips) or peripheral (hands/digits), cyanosis is quantified
as a bluish tinge to the skin commonly due to low levels of oxygen in the blood.
Accessory Muscle Use
These muscles are the sternocleidomastoids, the scalenes muscles, and the inter-
costals. Look for pronounced activity in these muscle groups, as it suggests the
patient is in respiratory distress and possible impending respiratory failure.
Paradoxical abdominal breathing
Abdomen moves in with inspiration, instead of moving out as it normally should.
This may be associated with respiratory distress.
Clubbing - See next page
INSPECTION
SECTION 1
57
Overview

• Although there are several hypotheses, ultimately the exact underlying pathophysiol-
ogy to clubbing is unclear. Clubbing is typically found in the fingers, but less com-
monly can also be seen in the toes.
Etiology
DDx of ClubbingDDx of Clubbing
Pulmonary • Lung cancer (primary or metastatic)
• Interstitial lung disease
• Bronchiectasis
• Cystic Fibrosis
• Lung abscess
• Tuberculosis
Cardiac • Endocarditis
• Atrial myxoma
• Congenital heart disease
GI • Inflammatory bowel disease
• Cirrhosis
Other • Hyperthyroidism
• Thalassemia
CLUBBING
SECTION 2
58
Pathophysiology

Examination
• Your general approach to the examination for clubbing is to first look for signs of
clubbing, and if present, then to perform a focused physical exam for the underlying
causes of clubbing.
• There are various methods described for the examination of clubbing. The nail fold
angle and phalangeal depth ratio are 2 evidence based approaches, while Scham-
roth's sign and nail-bed spongyness are historically described methods.
Examination for Clubbing
1. Nail Fold Angle
2. Phalangeal Depth Ratio
3. Schamroth's Sign
59

Nail Fold Angle (or Hyponychial Angle)
• Looking laterally at the digits, evaluate the nail fold angle
• 180 degrees is the mean normal nail fold angle
• Any nail fold angle >180 degrees is abnormal and suggestive of clubbing
60

Phalangeal Depth Ratio
• The Phalangeal Depth Ratio (PDR) is the ratio between the Distal Phalangeal Depth
(DPD) to Interphalangeal Depth (IPD). The DPD is the midpoint between the DIP
and the tip of the finger, while the IPD is the midpoint between the DIP & PIP joints.
PDR = DPD/IPD
• This is measured by observing the digits from the lateral view, ideally using calibers,
however practically most physicians use a visual estimation.
• In healthy patients, the IPD should be slightly greater than the DPD. Hence, the ratio
of the IPD to the DPD is rarely >1 in healthy patients, and in fact the mean phalangeal
depth ratio is noted as 0.9 in healthy patients.
• A Phalangeal Depth Ratio (DPD/IPD) of >1 suggests clubbing. In other words, this
means that the DPD is thicker and the IPD, hence the description of clubbing histori-
cally by some as drumstick-like fingers.
61

Schamroth's Sign
• This is performed by placing the dorsal aspects of similar fingers (usually the index
fingers) against each other.
• In healthy patients, the terminal phalanges should form a diamond-shaped window.
In patients with clubbing, there is no such diamond shaped window.
• There is no conclusive evidence for Schamroth's sign as a precise or accurate measure
of clubbing. It is still commonly used among practitioner's, however it is more of a
historic finding rather than one that is rooted in evidence based medicine.
Other Sign
• Nail-bed spongyness - this is performed by gently palpating the nail with the index
finger, while gripping the sides of the same index finger with the middle finger and
thumb. If during such palpation it is perceived that the nail is floating over the soft
tissue, then it is qualified as nail-bed spongyness and historically noted as being sug-
gestive of clubbing. There is however no conclusive data on this method, and it has
generally fallen out of favor as an objective method of detecting clubbing.
62

More Pictures of Clubbing
63

Overview
• When performing a full respiratory exam, after inspection you must always then
perform palpation. Palpation is comprised of 2 components:
1. Chest Excursion
2. Tactile Fremitus
• Note that palpation of the ribs or muscles involved in respiration is not performed
routinely.
PALPATION
SECTION 3
64

Chest Excursion
• Perform by placing both hands over the mid to lower back of the patient while having
the patient take deep breaths; your thumbs should be moving away from each other
equally during inspiration.
• The normal increase in distance between your thumbs during inspiration is roughly
5 cm.
• Any decrease in chest excursion below 5cm, or any asymmetric chest excursion
should be considered to be potentially a sign of pathology.
65
Video -Chest Excursion
Chest Excursion
o Bilateral decrease
✓COPD
✓ILD
o Unilateral decrease
✓Pneumonia
✓Pleural effusion
✓Pneumothorax

• Perform by placing the ulnar edge of both hands symmetrically over the posterior
chest, starting at the top where the apex of the lungs would be, and have the patient
say "99". You will be feeling for the vibration of sound upon your hands each time
the patient says "99". Repeat this for a total of at least 6 times to cover to extent of
the lung fields
• If the is any asymmetry detected in the vibration sense, or any change in intensity as
you proceed down the lung fields, then this suggests underlying pathology.
• If the vibration sense is increased during tactile fremitus, then this suggest pathology
involving an increase in solid material within the lung. This is because there is in-
creased conduction of sound through solids. This finding is typically associated with
pneumonia (consolidation in the form of pus).
• If the vibration sense is decreased during tactile fremitus, then this suggests an un-
derlying pathology involving an increase fluid or air. This is because there is de-
creased conduction of sound through fluid and/or air. This is typically associated
with pleural effusions or pneumothorax.
66
Tactile Fremitus
o Decrease
✓Pleural Effusion
✓Pneumothorax
o Increase
✓Pneumonia
Video - Tactile Fremitus
Tactile Fremitus

• After palpation, percussion must routinely be performed as part of the full respi-
ratory examination. This is done first over the back, then over the front of the
chest.
• During percussion you should be listening for whether the percussive sounds are
all of the same resonance bilaterally.
• If there is a sound that is different upon percussion, you should note whether it
is of increased resonance (hyperresonant), or decreased resonance (dull). You
should also note whether the change in resonance percussed is unilateral or bilat-
eral.
Percussion
o Hyperresonant
✓COPD
✓Pneumothorax
o Dull
✓Pneumonia/Consolidation
✓Pleural effusion
PERCUSSION
SECTION 4
67
Overview
Video - Percussion

Diaphragmatic Excursion
• Diaphragmatic excursion is a particular percussive technique that is no longer rou-
tinely performed as part of the respiratory examination, due to it being considered
generally to have a high level of variability between observers and is poorly vali-
dated.
• Diaphragmatic excursion is measured by percussing to determine the level of the
diaphragm posteriorly during inspiration (having the patient take a deep breath in
and holding, as you percuss the level), and comparing it to expiration. You would
measure the difference between these two levels, which gives you the diaphrag-
matic excursion. You would do this for one side, then repeat for the other side of
the chest wall.
• Normal is considered to be measured as 2 to 5cm. Note if there is any asymmetry.
A decreased or asymmetric diaphragmatic excursion may be a sign of underlying
lung pathology.
Diaphragmatic Excursion
o Decreased
✓COPD
✓Pneumonia
✓Pleural effusion
✓Paralyzed diaphragm
68

Approach
• Auscultation must routinely be performed as part of the respiratory examination,
first over the back then over the front of the chest. This helps with identifying po-
tential underlying lung pathologies.
• While auscultating, you should be listening for 2 things at each position:
1. Air entry
- is it present
- is it bilateral?
2. Abnormal sounds (adventitious sounds)
- Is there a wheeze?
- Are there crackles?
• Note that older textbooks differentiate between rales and rhonchi as forms of ad-
ventitious sounds. In fact, most physicians now agree that there is no difference
and both are now referred to simply as crackles.
AUSCULTATION
SECTION 5
69
Video - Auscultation

Aucultation
o Decreased Air Entry
✓COPD
✓Pneumonia
✓Pneumothorax
o Wheeze
✓COPD
✓Asthma
o Crackles
✓Pneumonia
✓Pulmonary edema
✓Interstitial lung disease
70

ILLNESS-SPECIFIC FINDINGS
SECTION 6
71
VITALS PALPATION PERCUSSION AUSCULTATION
COPD
exacerbation
hypoxia
tachypnea
Decreased chest
expansion
Hyperresonant Wheeze
Pneumonia
hypoxia
tachypnea
fever
Decreased chest
expansion
Increased tactile
fremitus
Dullness
Decreased air entry
Crackles
Pleural Effusion
hypoxia
tachypnea
Decreased chest
expansion
Decreased tactile
fremitus
Dullness Decreased air entry
Pneumothorax
hypoxia
tachypnea
hypotension (if
tension)
Decreased chest
expansion
Tracheal deviation
Hyperresonant Decreased air entry

ABDOMINAL EXAM
CHAPTER 4
72
Overview
Percussion
Auscultation
Inspection
• Distention
• Bulging
• Scars, Striae, Dilated veins, Bruising
• General Auscultation
• Auscultation for Bruits & Rubs
• Tympanic vs Dull
Palpation
Special Tests
• Light & Deep Palpation for:
• Pain
• Tone
• Guarding
• Rebound
• Hepatomegaly
• Splenomegaly
• Ascites
• Other

Step 1 - Introduction
• Wash hands
• Introduce yourself & what you are going to perform
• Always stand on patient’s right side for examination
Step 2 - Lighting, Draping, Positioning
• Appropriate lighting
• Ask if the patient is agreeable to having you turn on the overhead
lights
• Appropriate draping of the patient
• Start by covering the area below the waist with linen
• Expose abdomen by lifting gown upwards
• Appropriate positioning of the patient
• Patient lying flat with arms at the side
• Relax patient’s abdominal wall muscles by having them slightly flex
knees
PREPARATION
SECTION 1
73

Distension
Any time you inspect an abdomen, you should always routinely comment in your re-
port on whether the abdominal contour was distended or non-distended. To best
observe any distension, it is advisable to stand at the foot of the bed or position your-
self at the level of the abdomen.
Special Findings
You do not necessarily need to routinely report the following negative findings in
an otherwise healthy patient. However, you must absolutely comment on their pres-
ence or absence if they are pertinent to your patient's presentation.
• Bulging
• Bulging flanks - can be indicative of ascites
• Hernia - usually either peri-umbilical or inguinal
• Bladder distension - due to outlet obstruction or neurogenic bladder
• Abdominal aneurysm
• Visible peristalsis - indicative of possible bowel obstruction
• Striae (stretch marks)
• Pink - recent
• Silver - old/obese
• Purple- Cushing’s
• Scars
• If present, ask the patient about their etiology (trauma vs surgery)
• Dilated veins
• Caput medusae - seen in portal hypertension/cirrhosis
• Bruising
• Cullen’s sign & Grey-Turner’s sign - seen in pancreatitis
• Non-specific bruising from trauma, coagulopathy, or injection of heparin
INSPECTION
SECTION 2
74

Generally, the proper auscultation method for the abdominal exam:
1. Listen to each abdominal quadrant with the diaphragm of stethoscope
placed gently on the abdomen, without any pressure other than the force of
gravity being applied to the diaphragm of the stethoscope.
2. Listen on average for 15 to 30 seconds, although if you do not hear any
bowel sounds during this period, you need to listen for 2 to 5 minutes be-
fore definitely being able to conclude the absence of bowel sounds.
3. Note frequency of sound:
• Normal bowel sound are described as clicks and gurgles
• Increased: seen with diarrhea or early intestinal obstruction
• Decreased then absent: seen with ileus and peritonitis
AUSCULATION
SECTION 3
75
Overview of Auscultation
Note:
Auscultation is performed before percussion and palpation for the ab-
dominal exam, unlike when examining other systems, where the usual
pattern is IPPA (inspection, percussion, palpation, auscultation). This is
due to the fact that any palpation to the abdomen prior to auscultation
may cause an increase in bowel motility & bowel sounds, hence biasing
your results on auscultation.
Video - Abdominal Auscultation

Renal Bruits
• Renal bruits are classically described as a sound heard emanating from the re-
nal arteries, and the presence of a renal bruit suggest renal artery stenosis.
• Although auscultating for renal bruits is not necessarily a routine part of the ab-
dominal exam in an otherwise healthy patient, you must examine for a renal
bruit in any patient presenting with hypertension in particular. This is be-
cause a renal bruit may be suggestive of renal artery stenosis, and renal artery
stenosis is a secondary cause of hypertension.
• Classically we have been taught to examine for renal bruits by auscultating with
the diaphragm of the stethoscope 2-3 cm above the umbilicus, and 2 to 3 centi-
meters to either side. While auscultating for renal bruits you must actually
press quite firmly on the stethoscope in order to optimize your chances of hear-
ing the bruit.
• It is important to note that new evidence from the JAMA Rational Clinic Exam
on Renal Bruits argues that one may actually auscultate in any location of the 4
quadrants of the abdomen to hear a renal bruit.
76
Video - Abdominal Bruits

Evidence Based Medicine
JAMA RCE:
Is Listening for Abdominal Bruits Useful in the Evaluation of Hypertension?
JAMA Oct 25, 1995 Vol. 274 No. 16
Patient Population - The article reviews studies on young patients without history
of hypertension, older patients and also patients with documented intra-
abdominal arterial disease.
Comments:
• Since the kidneys lie retroperitoneal and the renal arteries leave the aorta in the
area cephalad to the umbilicus, attention should be given to auscultation in the
epigastric area for the bruit of renovascular disease, a pancreatic neoplasm, or
an innocent bruit
• The bruit of a hepatic carcinoma has been heard in the right upper quadrant,
while that of a splenic arteriovenous fistula has been described in the left up-
per quadrant.
• Periumbilical bruits are at times heard in the setting of mesenteric ischemia,
and venous hums are from portosystemic hypertension
• In older populations, an abdominal bruit may be associated with an abdominal
aortic aneurysm
• Renal bruits are seldom auscultated in patients with essential hypertension, but
substantial prevalence in young patients with renovascular disease
77

1. Place the 3rd digit of your left hand on the abdomen
2. The rest of your hand should not be touching the patient
3. Then tap the DIP of your 3rd digit, or alternatively the area just proximal to
the DIP, with the tip of your other hand’s 3rd digit
4. Do not rest your finger on your DIP at the end of tapping since it may alter the
quality of the sound. Instead release your finger upon percussion of your DIP
5. In terms of percussion sequence, you can ask the patient where it hurts most
and percuss that quadrant last
6. Percuss all 4 quadrants mainly for sound, but also note any pain:
• Normal sound to percussion: Tympany
• Abnormal: Dull, generally due to fluid (ascites) or feces (constipation)
• Note that a distended abdomen that is tympanic throughout suggests
bowel obstruction
PERCUSSION
SECTION 4
78
Overview of Percussion
Video - Abdominal Percussion

Overview of Palpation
1. Ask where it hurts and palpate that quadrant last
2. Keep your right hand horizontal and flex your fingers gently as you palpate
3. Lift your hand completely off between quadrants
4. Do the above first with light palpation, and then repeat with deep palpation
5. While palpating each of the 4 quadrants of the abdomen, look for:
• Pain - look at patient's facial expression while palpating to detect pain
• Tone - maximum tone is board like, and indicative of surgical peritonitis
• Guarding - may be indicative of peritonitis
PALPATION
SECTION 5
79
Video - Abdominal Palpation

Rebound Tenderness
• Once you've completed your light and deep palpation, you should then pro-
ceed to palpating for rebound tenderness, especially in patients presenting
with abdominal pain or gastrointestinal symptoms. The presence of re-
bound tenderness is suggestive of peritoneal inflammation/peritonitis.
• Rebound tenderness is performed by pressing your fingers firmly and slowly
and then quickly withdrawing on an area of the abdomen that DOESN’T
hurt. If the patient has more pain on release of pressure, then this is posi-
tive for rebound tenderness.
• Rebound tenderness in a patient with a very firm (board-like) abdomen to
palpation suggests surgical peritonitis (or secondary bacterial peritonitis),
and is a surgical emergency since it suggests possible underlying bowel perfo-
ration. Examples include patients with appendicitis or diverticulitis.
• Rebound tenderness in patient with an abdomen that is distended yet soft to
palpation suggests spontaneous bacterial peritonitis (SBP), which is not a
surgical emergency and is treated medically. SBP is secondary to ascites
from portal hypertension, often within the context of cirrhosis. SBP is
treated medically and is not a surgical emergency.
80

Test Technique Associated Pathology
Murphy’s Sign Place Fingers under coastal margin on
right side at mid-clavicular line and
have the patient to a deep breath while
you push. Arrest of deep inspiration
will cause pain.
Cholecystitis
Psoas Test Pain on flexion of hip against resistance Inflammation or abscess of
psoas muscle
Obturator Test Pain when thigh is flexed to right angle
and gently rotated first internally and
then externally
Inflammation of obturator
muscle (ie. appendicitis,
divertculitis, PID)
Rovsing’s sign RLQ pain on palpation of LLQ due to
gas movement
Appendicitis
SPECIAL TESTS
SECTION 6
81

• Liver size correlates with body size. Liver span is usually greater in men than
women, and in tall versus short individuals. However, as a rough guide, a liver
span of less than 12 cm makes hepatomegaly unlikely.
HEPATOMEGALY
SECTION 7
82
Hepatomegaly EtiologiesHepatomegaly Etiologies
Cirrhotic • Any cause of cirrhosis
Neoplastic
• Hepatocellular carcinoma
• Leukemia
• Lymphoma
Infectious
• Infectious Mononucleosis
Cardiac
• Right heart failure
Overview
Etiology

• Standing at the foot of the bed, inspect for any asymmetry. Any bulging or full-
ness in the right upper quadrant area may suggest hepatomegaly.
1. In adults without a history or physical findings suggestive of liver disease, start by
palpating for the lower liver edge.
2. Start with gentle pressure in the right lower quadrant in the midclavicular line
3. Ask the patient to gently take deep breaths in & out, which should move the liver
edge down and for it to be felt with the examiners fingertips, particularly in hepa-
tomegaly.
4. After each deep breath, move the fingers up roughly 2 cm & repeat the above.
5. If the liver edge is not felt by the time the examiner has palpated up to the costal
margin, then hepatomegaly is unlikely and no further physical examination is sug-
gested.
6. If the liver edge is felt, mark the location where the lower edge was felt and then
proceed to percussion
83
Inspection
Palpation

1. Note that percussion should only be performed if the liver edge is felt on palpa-
tion. If it is indeed felt, then begin percussion at the level of the third rib space, at
the midclavicular line.
2. Move down one rib space at a time until the tone of your percussion changes, in
terms of an increase in dullness to percussion. This is due to the interposition of
the dome of the liver behind the lung.
3. Once you do hear dullness to percussion, confirm it by spreading 2 to 3 fingers
over adjacent rib spaces and percuss quickly over your fingers from greater to
lesser resonance.
4. If doubt still persists, have the patient take a deep breath and hold it, then per-
cuss again as described above to confirm dullness at that rib interspace.
84
Percussion

JAMA RCE:
Physical Examination of the Liver. Naylor. JAMA, June 15, 1994
Comments:
• In patients with low probability of liver disease, the first step in examina-
tion of the liver should be palpation to locate the lower liver border in the
mid-clavicular line. If the liver is not palpable, then you can forgo any fur-
ther examination and defensibly conclude that there is no hepatomegaly.
• A palpable liver is not necessarily enlarged or diseased, but does increase
the likelihood of hepatomegaly.
• In situations where there is a palpable liver edge, then percussion is recom-
mended as the next step in the examination in order to ascertain the liver
span. A liver span of less than 12 to 13 cm reduces the probability of hepa-
tomegaly.
• In patients with a high probability of liver disease who have an impalpable
liver, it is recommended to proceed to percussion to measure liver span.
• Auscultation over the liver has a limited role and is seldom helpful.
• In terms of numbers, liver palpation is roughly 80% sensitive for detecting
hepatomegaly. Although the scratch test is more sensitive at roughly 85%,
it is not as specific of a test for hepatomegaly as palpation, especially in
patients who are overweight or with ascites.
85

Anatomy
• The spleen is an organ located in the left upper quadrant of the abdomen, deep within
the lateral ribcage, behind the stomach, and below the diaphragm.
• The spleen is not usually palpable in most healthy adults.
• The spleen participates in cellular and humoral immunity, as well as the removal of
senescent red blood cells. The spleen is also involved in removal of certain bacteria
from the circulation. In hyposplenism or asplenia, the patient will be more suscepti-
ble to bacterial sepsis, especially by encapsulated organisms.
Encapsulated Organisms
• Strep Pneumonia
• H. influenzae
• Neisseira meningitides
• Klebsiella
• Normally, about one-third of circulating platelets are sequestered in the spleen,
where they are in equilibrium with circulating platelets. Patients with splenomegaly
may have significant degrees of thrombocytopenia (with or without leukopenia and
anemia), but rarely have clinical bleeding, since their total platelet mass is usually
normal.
• The spleen also removes particles from within circulating red cells, such as nuclear
remnants (which are called Howell-Jolly bodies) & insoluble globin precipitates
(called Heinz bodies). Of clinical importance, Howell-Jolly bodies appear in circulat-
ing red cells when the spleen has been surgically removed or when there is splenic
dysfunction (ie. hyposplenism from infarction).
SPLENOMEGALY
SECTION 8
86
Physiology

87
Findings
Hyposplenism/
Asplenia
• Infection from encapsulated organisms
• Howell-Jolly bodies
• Heinz bodies
Splenomegaly • Thrombocytopenia
• Anemia, Leukopenia, or Leukocytosis
(less common, unless malignancy)
Major Causes of SplenomegalyMajor Causes of Splenomegaly
Hematologic/
Neoplastic
• Leukemia
• Lymphoma
• Multiple myeloma
• Myelofibrosis
• Polycythemia vera
• Essential thrombocytosis
• Sickle cell disease
• Metastatic tumors
Infectious Viral:
• EBV (infectious mononucleosis)
• CMV
• HIV
Bacterial:
• Endocarditis
• Tuberculosis
Parasitic:
• Malaria
• Schistosomiasis
Congestive • Right Heart failure
• Cirrhosis
• Thrombosis of portal, hepatic, or splenic veins
Etiologies for Splenomegaly

• According to the original JAMA article on splenomegaly, when inspecting for sple-
nomegaly, begin by percussion. The method of percussion with the highest sensitiv-
ity (roughly 85%) for the detection splenomegaly is a positive Castell’s sign. If Cas-
tell’s sign is positive, it suggests splenomegaly, then you must proceed to palpation
for further assessment of degree of splenomegaly. If Castell’s is negative, then you
can end your splenic examination, as splenomegaly is unlikely.
• Alternatively, in a recent JAMA update it has been suggested that Nixon’s method
may be the preferred initial test for splenomegaly. In this JAMA update, it is recom-
mended to begin with examination for Nixon’s method. If Nixon’s is positive, no fur-
ther testing with palpation is recommended.
• In summary, when examining for splenomegaly, the evidence suggest you should be-
gin with percussion. There are 3 different percussion methods (outlined below), how-
ever the evidence suggests using either Castell's sign or Nixon's method.
3 methods of percussion for splenomegaly
1. Percussion of Traube’s space
2. Castell’s sign
3. Nixon’s method
• If percussion is negative using Castell's sign or Nixon's method, then the evidence
(as per the JAMA RCE articles, see page 94) suggests you can stop your examination
for splenomegaly and conclude that it is unlikely. However, if percussion with either
Castell's or Nixon's is positive, then you must proceed to palpation, using one of the
methods outlined below:
3 methods of palpation for splenomegaly
1. Patient supine
2. Patient in right decubitus
3. Hooking
88
Overview of Splenic Exam

Percussion - Traube's Space
Technique:
1. Place the patient in the supine position, breathing normally
2. Locate Traube's space, which is a triangular area delineated by the left 6th
rib, the left costal margin, and the left anterior axillary line (or mid-axillary
line)
3. Percuss along Traube’s space, beginning midline and moving towards the
mid-axillary line.
Interpretation:
• Any dullness to percussion within Traube’s space is a positive sign and sug-
gests splenomegaly.
• As per the JAMA RCE on Splenomegaly, percussion of Traube's space is not a
particularly useful test for detecting splenomegaly.
89

Technique:
1. Place the patient in the supine position & find Castell's point, which is
located in the lowest intercostal space (8th or 9th intercostal space) at the
point of intersection with the left anterior axillary line (or alternatively, it
has been described along the left mid-axillary line as well).
2. Continuously percuss Castell's point while the patient takes a full inspiration
and then full expiration.
Interpretation:
• If the percussive note does not change (ie. remains tympanic) then it suggests
the presence of a normal spleen, and Castell's sign is considered to be nega-
tive. If Castell's is negative, then splenomegaly is unlikely and you discon-
tinue any further exam of the spleen, as per the JAMA RCE on Splenomegaly.
• If the percussive note changes from resonant to dull at the end of inspiration,
and then back to resonant over the course of full expiration, then Castell's
sign is regarded as positive, and this suggests splenomegaly.
• This is because as the patient inspires, the spleen moves inferiorly along the
posterolateral abdominal wall. If the spleen is enlarged enough that the infe-
rior pole reaches the eighth or ninth intercostal space, a dull percussion note
will be appreciated, indicating splenomegaly.
• If Castell's sign is positive, you should then proceed to palpating for the
spleen. (See next section).
90
Percussion - Castell's Sign

Percussion - Nixon's Method
Technique:
1. Place the patient in the right lateral decubitus position.
2. Begin percussing at the midpoint of left costal margin (nipple line), and
continue percussion up in a perpendicular fashion in relation to the costal
margin.
Interpretation
• A positive test is dullness percussed over 8 cm above the costal margin.
• The JAMA RCE on Splenomegaly on suggests that Nixon's Method is both sen-
sitive and specific for detecting splenomegaly
91

Palpation of the Spleen
• Note that overall, as the spleen enlarges it moves anterior and inferiorly.
• As a general rule, the spleen is only palpable when enlarged.
• Patient supine:
1. Start in RLQ and move up to LUQ
2. Pt inspires, and feel for spleen tip meeting examiner's stationary hand.
3. If not felt, move 2cm towards LUQ on expiration. 
• Patient in right decubitus:
1. Examiner's left hand is across patient's thorax, lifting the left ribcage
anteriorly and medially.
2. Right hand is just below costal margin.
3. Patient takes deep breath, and feel for spleen tip.
4. If not felt, move 2cm towards umbilicus to ensure massive spleen not
missed.
• Hooking:
1. Pt lies flat with fist under CVA on left.
2. Examiner is on patient's left side, facing patient's feet, with fingers of both
hands under costal margin.
3. Patient takes deep breath, and feel for tip.
92

JAMA RCE:
Does This Patient Have Splenomegaly?
Grover et al, JAMA, November 10, 1993
Patient Population - There were 7 studies that were compared. Studies con-
sisted of inpatients with and without splenomegaly, as well as patients with
alcoholism in one study.
Comments:
• The bedside examination of the spleen should start with percussion via Cas-
tell's sign (sensitivity of 80%, specificity of 82%). If percussion is not dull
(negative Castell’s sign), then there is no need to palpate because the re-
sults of palpation will not effectively rule in or rule out splenic enlarge-
ment.
• In the presence of a positive Castell’s sign, palpation should follow. The
sensitivity ranges anywhere from 20% to 70% among the 7 studies which
were examined, while specificity was >90% in 6 of the 7 studies looked at.
• If palpation is negative, then diagnostic imaging (ie. ultrasound) will be
required to confidently rule in or rule out splenomegaly.
• If both percussion and palpation are positive, then the diagnosis of sple-
nomegaly is established.
93

94

• Ascites is defined as an accumulation of fluid within the peritoneal cavity, most
commonly encountered as a result of portal hypertension from cirrhosis.
Etiology
• It is important to note that the approach to the differential of ascites is often first
based upon the Serum Album to Ascites Gradient (SAAG).
SAAG Overview
SAAG = Serum Album - Ascites Albumin
SAAG > 11 (1.1) = Portal Hypertension/Cirrhosis
SAAG < 11 (1.1) = Malignancy/Peritonitis/Pancreatitis
• A SAAG of greater than 11 is related to underlying portal hypertension. Think of
this as being similar in underlying physiology to a transudative effusion.
• A SAAG of less than 11 is not related to any underlying portal hypertension.
Think of this as being similar to an exudative effusion.
Common Causes of Ascites
1.Cirrhosis (most common)
2. Malignancy
3. Right Heart Failure
ASCITES
SECTION 9
95
Anatomy

Overview of Examination for Ascites
• Inspection for ascites follows the same general template as most other physical ex-
aminations, in the order of inspection, palpation, percussion. However, auscultation
is not a part of the exam for ascites. Specifically, the exam for ascites involves 4 com-
ponents: bulging flanks on inspection, flank dullness to percussion, and on palpation
you would perform 2 special tests known as the fluid wave and shifting dullness.
4 Components of Ascites Exam
1. Bulging flanks
2. Flank dullness to percussion
3. Fluid wave
4. Shifting dullness
• If examination for ascites is positive, then the next step is to further investigate with
either an abdominal ultrasound or CT scan to confirm findings.
96

Inspection - Bulging Flanks
• Inspect for abdominal distension. The most sensitive exam finding on inspection for
ascites is bulging flanks.
97

Percussion - Flank Dullness
• On percussion for ascites, you should percuss for flank dullness. This is performed by
beginning percussion from the midline of the abdomen and percussing laterally all the
way into the flank area. While percussing you should listen for any dullness. The ex-
amination is positive if there is dullness to percussion of the flanks.
• Flank dullness is the most sensitive finding on percussion for ascites.
98

Special Test - Shifting Dullness
• Shifting dullness
-note where percussion note becomes dull and mark on skin. Roll patient toward side
where the mark was placed (often easier to mark and roll patient to opposite side of exam-
iner). Allow 1 minute to pass and re-percuss abdomen. Positive if level of dullness changes
up toward the midline.
99

Special Test - Fluid Wave
• Fluid wave - with the edge of the patient’s/helper’s hand on the abdominal midline,
place both hands on either flank. One hand taps sharply with pads of fingers onto one
flank while the other hand waits to feel impulse on the other. Positive if impulse noted
with receiving hand after tap.
100

Other Special Tests
Other Tests (you can leave these out):
• Puddle sign is cruel and unusual - do not perform!
• Auscultatory percussion is neither sensitive nor specific
101

102
JAMA RCE:
Does This Patient Have Ascites?
Williams & Simel, JAMA, May 20, 1992
Patient Population - Male Veteran Inpatients
Comments:
• There is no single sign for detecting ascites that is both sensitive and specific.
• Flank dullness (84%) and bulging flanks (81%) had the highest sensitivity
• The fluid wave was the only sign with a high specificity (90%).
• The puddle sign performed poorly (sensitivity 55%).
• The most sensitive findings for ascites are bulging flanks, flank dullness, and
shifting dullness. Look for their absence to rule out ascites.
• The most specific findings for ascites are shifting dullness, fluid wave, and
peripheral edema. Look for their presence to rule in ascites.

• Romberg
• Cerebellar testing
• Finger-to-nose
• Rapid Alternating
• Pronator drift
NEUROLOGICAL EXAM
CHAPTER 5
103
General
Tests
• Cranial Nerves
• Motor
• Bulk
• Tone
• Strength
• Sensory
• Light Tough
• Vibration
• Proprioception
• Temperature
• Reflexes
• Gait
Special
Tests
Overview

Cranial Nerve I - Olfactory Nerve
• Not routinely tested
1) Visual Acuity:
1. Use a hand-held eye chart or Snellen’s chart on the wall. If a hand-held eye
chart is used, ask the patient to hold it 14 inches from the eyes. If a Snellen
chart is used, the patient must stand 6 metres from the chart.
2. Ask the patient to cover one eye and read progressively smaller lines until no
longer able to.
3. Test each eye separately.
2) Visual Fields:
1. Remove the patient’s eyeglasses.
2. Stand approximately 1 metre in front of patient. Your head should be level with
the patient’s.
3. Ask the patient to cover their right eye. Cover your left eye. Ensure the patient
looks into your uncovered eye while testing visual fields.
4. Using either a pen or your fingers, start moving from the periphery towards the
central field of vision in a diagonal fashion, and ask the patient to identify when
they see the pen or your fingers.
CRANIAL NERVES
SECTION 1
104
Cranial Nerve II - Optic Nerve

• Another viable method for testing visual fields is going through each of the 4 vis-
ual quadrants and asking the patient to tell you how many fingers you are hold-
ing up in each quadrant.
3) Fundoscopy: (usually deferred)
1. Dim the lights and ask the patient to fixate on a distant target.
2. Search for the optic disc (normally a yellow shallow cup with a clearly outlined
rim).
3. Examine for abnormalities such as papilloedema, optic disc atrophy (pallor), exu-
dates and hemorrhages.
4) Pupillary Light Reflex:
• CN II: Afferent
• CN III: Efferent
1. Ensure the lights are dimmed.
2. Inspect the pupils for size, shape and asymmetry.
3. Ask the patient to fixate on a distant target.
4. Approaching the patient from the side, shine a penlight into one of the pupils and as-
sess its reaction to light. Observe for pupillary constriction in the same eye (direct re-
sponse) and in the opposite eye (consensual response).
105

Cranial Nerves III, IV, VI
• This collection of cranial nerves are often referred to as the nerves of the extra-ocular
muscles, and are composed of:
• Cranial Nerve III (Oculomotor)
• Cranial Nerve IV (Trochlear)
• Cranial Nerve VI (Abducens)
• CN IV innervates Superior Oblique Muscle - moves eye down and in
• CN VI innervates Lateral rectus - moves eye laterally outwards
• CN III responsible for all other EOM innervation and movements
• CN III lesions causes:
• Eye position down and out
• Ptosis
• Pupillary Dilatation
Motor - Extra-Ocular Muscles:
1. Inspect the eyes for position and ptosis.
2. Smooth pursuit: Without moving their head, ask the patient to follow a target such as
a pen or finger in an “H” pattern. Note any failure of movement of either eye. Ask the
patient to report if diplopia occurs.
3. Nystagmus: Observe for involuntary rhythmic eye movements.
Reflex - Pupillary Light Reflex & Accomodation:
• Pupillary Light Reflex (CN II & III):
1. Ensure the lights are dimmed.
2. Inspect the pupils for size, shape and asymmetry.
3. Ask the patient to fixate on a distant target.
106

4. Approaching the patient from the side, shine a penlight into one of the pupils and as-
sess its reaction to light. Observe for pupillary constriction in the same eye (direct re-
sponse) and in the opposite eye (consensual response).
• Accomodation Reflex:
1. Ask the patient to look into the distance and focus on your finger at a distance.
2. Bring your finger towards the tip of their nose.
3. Pupils should constrict and eyes should converge
107

Cranial Nerves V - Trigeminal Nerve
Motor (V3 division) - Muscles of mastication
• Temporalis and Masseter:
1. Inspect for wasting of temporalis and masseter muscles.
2. Ask the patient to clench the teeth.
3. Palpate for contraction of the masseter and temporalis.
• Pterygoids:
1. Ask the patient to open their mouth.
2. Attempt to close the mouth with upward pressure on the jaw. Ask the patient to re-
sist you. The jaw will deviate to the weak side if a unilateral lesion is present.
Sensory:
• Light touch - V1, V2, V3
1. Ask the patient to close their eyes.
2. With a piece of cotton, touch the patient’s skin in the V1, V2 and V3 cutaneous distri-
butions of the nerve. Compare both sides.
Reflex:
• Corneal Reflex:
CN V: Afferent Limb of Corneal Reflex
CN VII: Efferent
1. Take a piece of tissue paper
2. Gently touch the cornea of the eye with the tip of the tissue paper
3. Observe for any involuntary blinking of both eyes. Stimulation of the corner should
cause an involuntary blinking reflex, which is the corner reflex.
4. Repeat above for the opposite eye.
108

In terms of pathology within the corneal reflex:
• Afferent defect: No blink in same or opposite eye.
• Efferent defect: No blink in same eye, but blink in opposite eye.
109

Cranial Nerve VII - Facial Nerve
Motor - Muscles of Facial Expression
• Inspect the face for asymmetry
• Ask the patient to raise their eyebrows (frontalis)
• Ask the patient to close their eyes tightly. Attempt to pull their eyes open and ask them
to resist you. (orbicularis oculi)
• Ask the patient to show you their teeth. Then ask them to close their mouth tightly. At-
tempt to pull their lips open and ask them to resist you. (orbicularis oris)
• Ask the patient to show you just their bottom teeth. (platysma)
Sensory:
• Taste for Anterior 2/3 of Tongue
Reflex:
• Corneal Reflex - efferent component - See previous section
110

Sensory - Hearing
1. Lightly rub your fingers next to each ear.
2. Ask the patient whether they can hear the sound, and whether it is equal
3. If hearing loss is suspected, perform Rinne’s and Weber’s tests (use tuning fork)
111
Cranial Nerve VIII - Vestibulocochlear

Cranial Nerve IX - Glossopharyngeal
Sensory:
• Taste for Posterior 1/3 of Tongue (CN IX)
Reflex:
• Gag Reflex (CN IX & X):
CN IX: Afferent limb of gag reflex
CN X: Efferent limb of gag reflex
1. With a tongue depressor, touch the soft palate on each side. A reflex contraction of
the soft palate should be noted.
2. If contraction is absent but sensation is normal, this suggests a CN X palsy. The gag
reflex is absent on the affected side.
112

Motor:
• Palatal Elevation (CN X):
1. Ask the patient to open their mouth and say ‘Ahhh’
2. Observe for displacement of the uvula
3. The uvula deviates to the non-affected side (ie: a unilateral right sided CN X palsy re-
sults in deviation of the tongue to the left)
• Articulation and Phonation (CN X):
• Assess patient’s speech for hoarseness
• Ask the patient to say “Ka, Ka, Ka” (palatal articulation)
• Ask the patient to say “Go, Go, Go” (guttural articulation)
• Ask the patient to say “Pa, Pa, Pa” (labial articulation)
113
Cranial Nerve X - Vagus

Motor:
• Trapezius:
• Ask patient to shrug the shoulders against resistance.
• Sternocleidomastoid Muscles:
1. Ask patient to turn their head to either side against resistance.
2. Observe and palpate the sternocleidomastoid muscles.
3. Remember that the right CN XI controls the right SCM, which turns the head to the
left. Therefore pathology in the right CN XI will produce an inability for the patient
to turn their head to the left.
114
Cranial Nerve XI - Accessory

Motor:
• Muscles of the tongue:
1. Observe the tongue at rest for fasciculations
2. Ask the patient to stick out their tongue.
3. Observe for deviation of the tongue to one side. The tongue deviates to the weaker
side, which is the side of the lesion.
115
Cranial Nerve XII - Hypoglossal

Overview
3 Components of Motor Exam
1. Muscle Bulk
2. Muscle Tone
3. Muscle Strength
There are 3 components to the motor exam (in order); inspection for muscle bulk,
followed by examination for muscle tone, and finally muscle strength (or power).
One of the most common mistakes made by medical learners in the motor exam is
that they ignore examining for bulk & tone, and jump directly to examining for mus-
cle strength. Please avoid this common error.
MOTOR
SECTION 2
116

Muscle Bulk
• Muscle bulk is determined based on inspection. Overall you would be inspect-
ing all the major muscles of the limbs looking for any evidence of loss of muscle
bulk, which is a sign of possible lower motor neuron injury.
• For example, in the upper limbs you would be looking for squaring of the shoul-
ders, which is a sign of deltoid muscle atrophy. Interosseous muscle wasting of
the hands is another site where loss of muscle bulk can be evident. Other promi-
nent muscles in the upper limbs that can be assessed are the biceps and triceps,
however loss of bulk in these muscles can be more difficult to assess.
• In the lower extremities, look for loss of bulk in the quadriceps muscles, which is
fairly easily identifiable in the form of "scooping" within the medial area of the
thighs.
117

Muscle Tone
• Muscle tone must be examined both in the upper and lower extremities.
• In the upper extremities (arms), tone is often determined with a back and
forth flexion & extension that is performed concomitantly at the level of
the wrists and elbows. See video:
• In the lower extremities (legs), tone is simply determined by flexing and
extending the knees in a repetitive fashion. This is then repeated for the
ankles. See video:
• What you are essentially looking for when examining for tone are changes
in resistance. An increase in resistance in relation to baseline is noted as
an increase in tone, while a decrease in resistance in relation to baseline is
noted a a decrease in tone. Being able to note whether tone is abnormal
simply comes with practice. Only after you have examined many patients
with normal tone can you then note when tone feels increased or de-
creased, especially when findings are subtle. Hence why you should rou-
tinely perform thorough neurological exams in all your patients.
• Tone is typically increased in upper motor neuron disease, common exam-
ples being stroke, Parkinson's disease, or Multiple Sclerosis.
• Tone is typically decreased in lower motor neuron disease, such as in any
peripheral neuropathy, radiculopathy, or Guillain-Barre syndrome.
• It is important to note that there are two major types of increased tone:
spasticity and rigidity.
• Spasticity is an increase in tone that is unidirectional and velocity de-
pendent
• Rigidity is an increase in tone that is bidirectional and velocity inde-
pendent.
118

Muscle Strength
• Muscle strength, or power, must be routinely examined in all four limbs, starting with the
upper limbs and working your way down to the lower limbs.
• You would ask the patient to perform a movement, and while they are performing that
movement you would be applying resistance, in the form of an equal and opposite force.
The motor strength would be determined based on the patient's ability to both perform
the movement as well as resist the force that you are applying. This process should be
done concomitantly on both sides of the body, and should be started at the proximal limb
muscles and sequentially moving distally.
• For example, if testing for motor strength in the upper limbs, you would start by having
the patient abduct both shoulders while you apply an equal and opposite force. This move-
ment would be testing the deltoid strength, which you would note out of a scale of 5. Once
completed, you would repeat the above for the the biceps muscles, the triceps, and so on.
MOTOR
STRENGTH
DEFINITION
5/5 Normal Strength
4/5
Muscle movement against gravity and
resistance, but not fully.
Broken down subjectively into 4-, 4, & 4+
3/5
Muscle Movement against gravity, but not
against resistance
2/5 Muscle Movement, but not against gravity
1/5 Muscle Flicker, No Movement
0/5 No Muscle Contraction
119

Upper Extremities Motor Strength:
NERVE
ROOT
MUSCLE MOTION
C5 Deltoid Shoulder Abduction
C6 Biceps Arm Flexion
C7 Triceps Arm Extension
C8
Intrinsic muscles of
the hands
Pinky Abduction
T1
Intrinsic muscles of
the hands
Thumb Abduction
Lower Extremities Motor Strength:
NERVE
ROOT
MUSCLE MOTION
L1-L2 Iliopsoas Leg Flexion
L3-4 Quadriceps Knee Extension
L5 Tibialis anterior Dorsiflexion
S1 Triceps surae Plantar Flexion
120

Overview
5 Components of Sensory Exam
1. Light Touch
2. Vibration
3. Proprioception
4. Temperature
5. Pain
On a routine neurological screening examination, you must always perform light touch.
However, the other 4 components of the sensory exam are not necessarily part of the rou-
tine sensory exam and are to be performed only when clinically warranted.
For example, a patient with diabetes in whom you are worried about diabetic neuropa-
thy, you will need to perform light touch but also examine for vibration and propriocep-
tion, particularly of the feet.
By contrast, a patient who is admitted to your service with pneumonia should have a full
screening neurological exam performed upon admission (in fact all of your patients
should), however you do not need to examine the other sensory modalities, outside of
light touch, if the patient is otherwise healthy.
SENSORY
SECTION 3
121

Overview
6 Major Reflexes
1. Biceps
2. Triceps
3. Brachioradialis
4. Patellar
5. Ankle
6. Plantar
• You must always perform all of the above 6 reflexes as part of a routine neuro-
logical examination. The first 5 are deep tendon reflexes. Note that the plan-
tar reflex used to be called the Babinski reflex.
• As a general rule whenever assessing any reflex, you must have the patient re-
lax the limb in question, otherwise you may have difficulty eliciting the reflex.
• If you are having difficulty eliciting a reflex, despite the patient having the limb
in question relaxed, then consider having the patient perform reinforcement
maneuvers. These will potentially help bring about the reflex. The two most
common are either having the patient clench their teeth, or alternatively have
the patient hook together their flexed fingers and pull them apart.
• You can describe reflexes as “absent,” “present,” “brisk,” or “hyperactive". Al-
ternatively, the below nomenclature is also used. If you have a hyperactive re-
flex don’t forget to look for clonus.
• 0: absent reflex
• 1+: trace, or seen only with reinforcement
• 2+: normal
• 3+: brisk
• 4+: hyperactive with non-sustained clonus
• 5+: hyperactive with sustained clonus
REFLEXES
SECTION 4
122

A Guide to the Physical Examination - By Dr. Sam Gharbi

A Guide to the Physical Examination - By Dr. Sam Gharbi

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