Advanced Assessment of the
Cardiovascular System
Mary Beerman, RN, MN, CCRN
NUR 602
Interesting facts...
The heart does not rest for more than a
fraction of a second at a time
 During a lifetime it contracts more than
4 billion times
 Coronary arteries supply more than 10
million liters of blood to the
myocardium in a lifetime

Interesting facts….
Cardiac output (heart rate X stroke
volume) can vary under physiologic
conditions from 3 to 30 liters/minute
 Remember: Normal cardiac output for
adults is 5-6 liters/minute
 Cardiac index corrects for body size
(Cardiac output divided by body surface
area)

Common Diseases of the
Heart
Coronary artery disease
 Hypertension
 Rheumatic heart disease
 Bacterial endocarditis
 Congenital heart disease

OTHER VERY COMMON
DISEASES OF THE HEART

CONGESTIVE HEART FAILURE

CARDIOMYOPATHY

ARRHYTHMIAS
Review Structure and
Physiology of the Heart in
textbook
Review of Symptoms
Chest Pain
This is the most important symptom of
cardiac disease
 Pain could be from pulmonary,
intestinal, gallbladder, or
musculoskeletal sources but it may be
from the heart itself
 Every complaint of chest pain must be
taken very seriously!

Differential Diagnoses of Chest
Pain








Angina
Myocardial Infarction
Other Ischemic C-V Origins
Non-ischemic C-V Origins
Pulmonary
Gastrointestinal
Psychogenic
Neuromusculoskeletal
Differential Diagnosis of Chest
Pain - ANGINA
 Usually
substernal
 Radiation – chest, shoulders, neck,
jaw,arms
 Deep, visceral (pressure) – intense,
not excruciating
 Duration- min., not sec. (5-15 min.)
Differential Diagnosis of Chest
Pain - ANGINA
Associated with nausea, vomiting
diaphoresis, pallor
 Precipitated by exercise & emotion
 Becomes Unstable when occurs during
sleep, at rest, or increases in
severity/frequency
 Relief with rest or NTG

Differential Diagnosis of CP –
Myocardial Infarction
Same type of pain as angina
 Duration greater than 15 min.
 Occurs spontaneously, often sequela of
unstable angina
 Relieved with Morphine, successful
reperfusion of blocked coronary artery

Differential Diagnosis of CP –
Other C-V Ischemic Origins
Aortic Stenosis/Regurgitation
 Idiopathic Hypertrophic Subaortic
Stenosis (IHSS)
 Uncontrolled Hypertension
 Severe Anemia/Hypoxia
 Tachycardia/Arrhythmias
 Pulmonary Hypertension

Differential Diagnosis of CP –
Nonischemic C-V Origins

Aortic Dissection
– Sudden, excruciating pain (knife-like,
tearing)
– Migrating pain (depends on location of
tear)
– Frequently, hemodynamic instability
– Appearance of shock with normal or
elevated BP
– Absent or unequal peripheral pulses
Differential Diagnosis of CP –
Nonischemic C-V Origins

Pericarditis
– Sharp or dull, retrosternal or precordial
pain
– Radiates to trapezius ridge
– Aggravated by inspiration, coughing,
recumbency, & rotation of trunk
– Lessened by sitting upright & leaning
forward
– Relief - analgesics & anti-inflammatory
meds
Differential Diagnosis of CP –
Nonischemic C-V Origins

Mitral Valve Prolapse
– Left anterior superficial, rarely
visceral pain
– Variable in character
– Lasts minutes, not hours
– Spontaneous onset with no pattern
– Relieved with time
Differential Diagnosis of CP Pulmonary
Pulmonary Embolus /Infarct
 Pneumothorax
 Pneumonia with pleural involvement
 Pleurisy

Differential Diagnosis of CP Pulmonary

Pleuritic Pain
– Visceral Pain arising from inferior portion of pleura
– May be substernal and radiate to costal margins or
upper abdomen
– Lasts greater than 30 minutes
– Often occurs spontaneously with associated
dyspnea
– Worsened with inspiration
– Relief – time, rest, bronchodilators
Differential Diagnosis of CP Gastrointestinal

Esophageal Spasm
– Substernal visceral (pressure) pain,
radiates
– Duration – 5 to 60 minutes
– Spontaneous or provoked by cold
liquids,exercise
– Mimics angina
– Relief with NTG
Differential Diagnosis of CP Gastrointestinal

GERD/Hiatal Hernia
– Substernal & epigastric, rarely radiates
– Duration is 10-60 min.
– Provoked by recumbency, lack of food
– Relieved by food, antacid

Peptic Ulcer Disease
– Substernal & epigastric pressure/burning
– Duration – hours
Differential Diagnosis of CP Gastrointestinal

PUD (Cont.)
– Precipitated by lack of food or “acidic” food
– Relief with antacids & food

Biliary Disease
– Colicky or continuous, visceral epigastric & RUQ
abdominal pain
– Radiates to back & right shoulder
– Occurs spontaneous & after heavy meal
– Relief – analgesics & time
Differential Diagnosis of CP Psychogenic
Nonradiating, variable pain over chest
 Duration – 2-3 minutes
 May be associated with
numbness/tingling of hands & mouth
 Precipitated by stress, emotional
tachypnea
 Relief by removal of stimulus, relaxation
 Causes – depression, anxiety, self gain

Differential Diagnosis of CP Neuromusculoskeletal
Thoracic Outlet Syndrome
 Degenerative Joint Disease of
cervical/thoracic spine

– Superficial pain in arms & neck
– Duration – variable, gradually subsides
– Precipitated by head & neck movement,
palpation
– Relief – time, analgesia
Differential Diagnosis of CP Neuromusculoskeletal

Herpes Zoster (Shingle’s)
– Pain follows dermatomal distribution of nerve

Costochondritis (Tietze’s syndrome)
– Superficial pain, reproducible with movement &
palpation
– May be localized or in multiple locations
– Duration – variable
– Relief – time, analgesia, anti-inflammatory meds
Ask These Questions about
Chest Pain
Description of character
 Location
 Duration/Recurrence
 Precipitating factors
 Associated symptoms
 Relieving factors
 History of similar symptoms

Angina
Angina Pectoris is the true symptom of
coronary artery disease.
 It is caused by hypoxia to the
myocardium which leads to anaerobic
metabolism and the production of lactic
acid. The acid irritates the actual heart
muscle and makes it hurt

Angina, con’t
Angina is due to an imbalance of
oxygen delivery TO the heart and the
oxygen needs OF the heart
 Levine’s Sign---Patients will describe
angina by clenching their first and
placing it over the sternum.

PALPITATIONS
Palpitations
The uncomfortable sensations in the
chest associated with a range of
arrhythmias.
 Patients may describe palpitations as
fluttering, skipped beats, pounding,
jumping, stopping, or irregularity

EXTRASYSTOLES
 Premature
atrial contractions
(PAC’s)
 Premature ventricular contractions
(PVC’s)
TACHYARRHYTHMIAS

Sinus Tachycardia
– Usually gradual onset and offset

Paroxysmal Supraventricular
Tachycardia (PSVT)
– Sudden, abrupt onset and offset
Atrial Fibrillation
 Ventricular Tachycardia

CAUSES of ATRIAL FIBRILLATION





Hypertension
Hyperthyroidism
Acute MI
Pericarditis
Coronary Artery
Disease




Congestive Heart
Failure
Valvular Heart
Disease
Acute or Chronic
ETOH abuse
Post-operative state
ATRIAL FIBRILLATION

Major complication
– Peripheral embolization
– CVA

May present as CVA, Transient ischemic
attack, Amaurosis fugax, ischemic limb,
ischemic bowel or other viscera
VENTRICULAR TACHYCARDIA

Causes include:
– Acute myocardial ischemia/infarct
– Chronic Coronary artery disease
– Cardiomyopathy
– Prolonged QT interval (Congenital, druginduced, acquired)
VENTRICULAR TACHYCARDIA

May present as:
– Sudden cardiac death

VT degenerated into VF
– Syncope
– Wide complex tachycardia

Often hemodynamically well tolerated
BRADY - ARRHYTHMIAS

Heart Block

Sinus Arrest
Common Causes of Palpitations DRUGS

Bronchodilators
– tachycardia

Beta Blockers, Calcium Channel
Blockers
– bradycardia

Digitalis
– bradycardia, toxicity causes bradydysrhythmias
Common Causes of Palpitations –
More DRUGS

Antidepressants
– Prolong QT interval

OTC medications – Antihistamines,
Decongestants, Weight Loss
preparations
– Extrasystoles, Tachy-dysrhythmias
Common Causes of Palpitations –
OTHER

Tobacco

Caffeine

Thyroid disorders
Paroxysmal Nocturnal
Dyspnea (PND)
Occurs at night or when patient is
supine.
 Patient awakens after being asleep
about 2 hours and is “smothering”.
Runs to window to get more air
 This is a specific sign of congestive
heart failure

Orthopnea
Dyspnea when lying down
 Ask all patients: “How many pillows do
you use in order to sleep?”
 To quantify the orthopnea, record “3pillow orthopnea for the past month”

Dyspnea on Exertion (DOE)
This is usually due to chronic CHF or
severe pulmonary disease
 Quantify the severity by asking, “How
many level blocks can you walk before
you get short of breath? How many
could you walk six months ago?”

How to Chart about Dyspnea

“The patient has had 1-block dyspnea
on exertion for the past six months.
Before 6 months ago, the patient was
able to walk 4 blocks without shortness
of breath. In addition, during the past
month the patient has noted 4-pillow
orthopnea. Previously he was able to
sleep with just two pillows.”
Common Causes of Congestive
Heart Failure
Uncontrolled Hypertension
 Myocardial ischemia/infarct
 Arrhythmias
 Lack of compliance

– Diet
– Drugs

Fluid overload
More Common Causes of
Congestive Heart Failure
Blood loss, Anemia
 Pulmonary embolism
 Systemic infection
 Valvular heart disease
 Nonischemic Dilated Cardiomyopathy
 Renal Artery Stenosis

SYNCOPE
Syncope
Fainting or syncope is the transient loss
of consciousness that is due to
inadequate cerebral perfusion
 Syncope can be from cardiac or noncardiac causes

Common Causes of Syncope
Cardiac
 Neurocardiogenic
 Orthostatic Hypotension
 Metabolic
 Neurologic
 Psychogenic

Common Causes of Syncope CARDIAC

Obstruction to Blood Flow
– Valvular stenosis
– Hypertrophic cardiomyopathy
– Prosthetic valve dysfunction
– Atrial myxoma
Common Causes of Syncope CARDIAC

Obstruction to Blood Flow (cont)
– Pericardial tamponade
– Pulmonary hypertension
– Pulmonary emboli
– Congenital heart disease
– Pump failure (MI or ischemia)
Common Causes of Syncope CARDIAC

Arrhythmias
– Brady-arrhythmias





Sinus bradycardia
Sick sinus syndrome
Atrioventricular block (AVB)
Pacemaker malfunction
Drug-induced bradycardia
– Tachy-dysrhythmias

VTach, SVT
Common Causes of Syncope NEUROCARDIOGENIC
Vasovagal
Vasodepressor
Carotid sinus hypersensitivity
Situational – Cough, Micturition, Defecation,
Deglutition
Vasovagal Syncope
This is the most common type of
fainting and is one of the most difficult
to manage.
 It has been estimated that 40% of all
syncopal events are vasovagal in nature
 This occurs during periods of sudden,
stressful, or painful experiences such as
getting bad news, trauma, blood loss,
sight of blood

Vasovagal Syncope, con’t

There is warning that the fainting is
about to occur…pallor, nausea,
weakness, blurred vision,
lightheadedness, perspiration, yawning,
diaphoresis, hyperventilation, or a
“sinking feeling”
Carotid Sinus Syncope
This may occur in the elderly who may
have a hypersensitive carotid sinus
 If they are wearing a tight shirt or collar
or turn their neck in a certain way,
there is increased stimulation of the
carotid sinus, a sudden fall in systolic
blood pressure, and a decrease in heart
rate.

Common Causes of Syncope –
Orthostatic Hypotension

Volume depletion

Antihypertensive medications

Antidepressant medications
Common Causes of Syncope –
METABOLIC

Hypoglycemia

Hyperventilation

Hypoxia
Common Causes of Syncope

NEUROLOGIC
– Epilepsy
– Cerebrovascular disease

PSYCHOGENIC
Ask These Questions about
Syncope
“What were you doing just before you
fainted?”
 “Have you had recurrent fainting spells?
How often do they happen?”
 “Was there an abrupt onset to the
fainting, or did you feel it coming?”
 “Did you totally lose consciousness?”

Syncope Questions, con’t
“In what position were you in when you
fainted?” (possible orthostatic
hypotension?)
 Was the fainting preceded by other
symptoms like nausea, chest pain,
palpitations, confusion, numbness, or
hunger?

…more syncope questions...
“Was fainting episode witnessed by
anyone? Who?
 “Did you have warning that you were
going to faint?”
 “Did you have any black, tarry BMs
before or after the fainting episode?
 “Did you experience any loss of urine or
stool during the fainting episode?”

And Just One More

“On regaining consciousness, did you
know where you were and who people
were around you?”
Fatigue
This is a common symptom of
decreased cardiac output. A common
complaint from people with CHF and
mitral valve disorder
 Fatigue may be the presenting
symptom of a woman having an MI
 Not at all specific to heart disease, but
you must consider it always

Common Causes of Fatique
Cardiac
 Anxiety/Depression
 Anemia
 Chronic Diseases

Dependent Edema
When peripheral venous pressure is
high, fluid leaks out from the veins into
tissues
 This is often the presenting symptom of
right ventricular failure
 Edema will begin in legs and gets worse
as the day progresses. Least evident in
the a.m. after sleeping with the legs
flat, worse as gravity pulls fluid to legs.

More about Dependent Edema




This indicates that there is excess fluid
volume and 3rd spacing of fluids.
People on bedrest will have edema of their
sacral area
In severe right or bi-ventricular heart failure,
people often have abdominal distension, liver
engorgement, constipation, and anorexia
Anasarca may develop. Gross generalized
edema
Ask These Questions about
Dependent Edema
“When did you first notice the
swelling?”
 “Do both legs swell equally?”
 “Did the swelling appear suddenly?”
 “What time of the day is it worse?”
 “Does it disappear after sleeping?”
 “Does propping your legs up make it go
away?”

More Questions about
Edema...
“What medicines do you take now?”
 “Do you have any kidney, heart, or liver
disease?”
 “Do you have shortness of breath? Pain
in your legs? Ulcers on your legs?”

And, More Questions about
Edema
Have you noticed a difference in how
your clothes fit, especially around the
waist?
 Have you noticed recent problems with
constipation?
 How is your appetite?

More and More
Do you add salt to food at mealtime
and/or when cooking
 Do you eat out in restaurants or get
take-out food frequently?
 Do you read labels on food before
purchasing?

Physical Exam for Edema
Press fingers into the dependent areas
for 2-3 seconds.
 If pitting is present, the fingers will sink
into the tissue and when fingers are
removed, the impression of the fingers
will remain
 Edema is quantified from 1+ to 4+
depending on how deep the indentation
is

The Physical Examination
Inspection
General Appearance
Is the patient in acute distress?
 Is breathing labored or easy?
 Is there use of accessory muscles?
 Is there cyanosis? Pallor?
 Are xanthomata present (stony hard,
yellowish masses on extensor tendons
of the fingers. Due to
hypercholesterolemia

Inspection...
Inspect nails. Splinter hemorrhages are
associated with infective endocarditis
 Inspect the face. People with
supravalvular aortic stenosis have wideset eyes, stabismus, low-set ears,
upturned nose, hypoplasia of the
mandible
 Moon face suggests pulmonic stenosis

More inspection...
Expressionless face with puffy eyelids
and loss of the outer 1/3 of the
eyebrow is seen in hypothyroidism
 Inspect eyes. Yellow plaques on eyelids
(xanthelasma) may be due to
hyperlipoproteinemia
 Opacities of the cornea may be
sarcoidosis

…and more inspection...
Conjunctival hemorrhage is commonly
seen with infective endocarditis
 Petechiae on the palate may be seen
with infectious endocarditis
 High arched palate may be seen with
Marfan’s Syndrome
 Arm Breadth greater that body height is
also seen in Marfan’s

Inspection of the Chest Wall
The heart and chest develop at the
same time in embryo, so anything that
interferes with development of the
chest may interfere with the heart
 Pectus Excavatum (caved-in chest) is
seen in Marfan’s syndrome and
sometimes MVP
 Pectus Carinatum (pigeon breast) also
seen in Marfan’s syndrome

Inspection of the chest, con’t

Are there any visible cardiac motions?
Inspection of the extremities
Look for edema (pitting and nonpitting)
 Observe color
 Babies with atrial septal defects may
have an extra finger or toe.
 Long, slender fingers suggest Marfan’s
with possible aortic valve deformity

Inspection of Extremities
Continued

Loss of hair may indicate
hypothyroidism or PVD
Assessment of Blood Pressure
Always measure in both arms sitting
 Then take BP standing

Orthostatic Hypotension
Have the patient lie down for 5 minutes
and measure BP and pulse
 Have patient stand and repeat reading
immediately. Allow 90 seconds for
maximum orthostatic changes
 A drop in systolic BP of 20 mmHg
or more when standing is
orthostatic
 There is usually an increase in HR

Rule out Supravalvular Aortic
Stenosis
If there is hypertension in the right
arm, take BP in the left arm as well
 In supravalvular aortic stenosis, there
will be hypertension in the right arm
and hypotension in the left arm

Rule out Coarctation of the
Aorta
If the patient is hypertensive in both
arms, have patient lie on abdomen, put
cuff around lower thigh, listen to BP at
the popliteal artery
 A leg blood pressure lower than the arm
BP suggests coarctation
 Normally BP higher in leg arteries than
arm

Rule out Cardiac Tamponade
An exageration of the normal
inspiratory fall in systolic BP (it should
normally fall about 5 mmHg during
inspiration
 You should check for a paradoxical
pulse any time there is low arterial BP
and a rapid, feeble pulse

Checking for Paradoxical Pulse
Have the patient breathe normally,
inflate BP cuff until no sounds are
heard.
 Gradually deflate cuff until sounds are
heard on expiration only and note this
number
 Continue to deflate the cuff until sounds
are heard during inspiration as well.
Note this number

A Positive Paradoxical Pulse

If the difference in BP exceeds 10
mmHg, this is abnormal and indicates
possible cardiac tamponade
Assessment of the Arterial
Pulse
Grasp both radial arteries, count for 30
seconds, and multiply by 2
 Determine rhythm. The slower the
rate, the longer you should palpate.
 If the rhythm is irregular, is there a
pattern to the irregularity?

Arterial Pulse, con’t
Premature beats are isolated extra
beats in a regular rhythm
 A grossly irregular rhythm is most likely
atrial fibrillation
 Palpate the carotid artery by standing at
the patients’ right side with him resting
on his back. Listen first for possible
bruit and do not palpate if you hear one

Arterial Pulse, con’t

Never palpate both carotids at the same
time
Jugular Venous Pulse
Remember that the internal jugular vein
provides information about right atrial
pressure
 The pulsation of the internal jugular
vein are beneath the
sternocleidomastoid muscle and are
visible as they are transmitted through
surrounding tissue
 The vein itself cannot be seen

Jugular Venous Pressure, con’t
Because the right internal jugular vein
is straighter than the left, only the right
IJV is evaluated
 To determine jugular waveform, have
patient lie without pillow at about 25
degree angle. Turn head slight to the
right and slightly down to relax the right
sternocleidomastoid muscle

Jugular Venous Pulse, con’t
Standing on the right side of the
patient, place your right hand holding a
pinlight on the patients sternum and
shine the light tangentially across the
right side of the patient’s neck.
 Shadows of the pulsation will be cast on
the sheet.
 Chart: “JV pulsation seen at 25
degrees”

Jugular Venous Distension
Hepatojugular Reflex
A useful test for assessing high jugular
venous pressure (also called abdominal
compression)
 By applying pressure over the liver, you
can grossly assess RV function. People
with RV failure have dilated sinusoids in
the liver. Pressure over right upper
quadrant pushes blood out and
increases JV pressure

How to Check for
Hepatojugular Reflex
Have patient lie in bed, mouth open,
breathe normally to prevent valsalva
maneuver.
 Place right hand over RUQ and apply
firm pressure for 10 seconds
 Normally there will be a short increase
in venous dilation followed by fall to
baseline

How to Check for Hepatojugular
Reflex – Cont.

If there is RV failure, neck veins will
stay elevated during entire time of
compression
Percussion
Not helpful in CV assessment
 CXR shows heart size and borders very
accurately

Palpation
Point of Maximal Impulse
(PMI)
Stand on the right side of the patient
with him sitting. Place fingertips at 5th
ICS, MCL and you should feel PMI
 PMI is usually within 10 cm of the
midsternal line and no larger than 2-3
cm diameter
 PMI that is lateral or displaced suggests
cardiomegaly

PMI, con’t
About 70% of the time you will be able
to feel PMI with patient sitting. If you
can’t, turn patient to his left side, lying
down.
 A PMI that is over 3 cm diameter
indicates left ventricular hypertrophy
and is 86% predictive of increased left
ventricular end diastolic pressure

General Motion
After palpating with the fingertips for
PMI, use palm of your hand to palpate
any large areas of sustained outward
motion (“heave” or “lift”)
 Palpate all 4 cardiac areas
 Any condition that increases the rate of
ventricular filling can produce a
palpable impulse

“Have you ever felt a thrill?”
Thrills are superficial vibratory
sensations felt on the skin overlying an
area of turbulence
 The presence of a thrill indicates that
you will hear a loud murmur (grade 46)
 Simply an indication of what you will
hear when you listen.

Auscultation
General Principles of
Auscultation
Close your eyes when listening
 Never listen through any kind of
clothing
 Listen at all 4 cardiac areas:

Aortic --2nd ICS, RSB

Pulmonic---2nd ICS, LSB

Mitral--cardiac apex, 5th ICS, MCL

Tricuspid---left lower sternal border

Principles of Auscultation,
con’t
Normally only the closing of valves can
be heard.
 Closure of the tricuspid and mitral
valves (AV valves) produce the 1st heart
sound.
 Closure of the aortic and pulmonic
valves produce the 2nd heart sound.
 Opening of valves can only be heard if
they are very damaged (opening “snap”

Third Heart Sound
When AV valves open, the period of
rapid filling of ventricles occurs. 80%
of ventricular filling occurs now. At the
END of rapid filling, a 3rd heart sound
may be heard
 S-3 is normal in children and young
adults, but not in people over age 30.
It means there is volume overload of
ventricle

What an S3 Sounds Like...

SLOSH-ing-in, Slosh-ing-in, Slosh-
ing-in
 Or Ken-tuck-y
Fourth Heart Sound
At the end of diastole, atrial contraction
contributes to the additional 20% filling
of the ventricle
 If the left ventricle is stiff and noncompliant, you will hear an S4.
 It sounds like this: a-STIFF-wall, aSTIFF-wall, a-STIFF-wall
 Or sounds like TEN-ne-see

Gallop Rhythms
The presence of an S3 and an S4
creates a cadence resembling the gallop
of a horse.
 Hence the term “gallop rhythm”

Auscultation Procedure
Stand at the patient’s right side while
he is flat on his back.
 Listen to all 4 valve areas, inching the
stethoscope along from area to area
 While listening at the apex and left
lower sternal border with the bell, you’ll
be able to determine if an S3 or S4 are
present

Procedures, con’t
Next have the patient turn to his left
side and listen to the apex for lowpitched diastolic murmurs with bell
 Have patient sit upright and listen
everywhere with diaphragm.
 Have patient sit and lean forward,
exhale, and hold breath while you listen
with diaphragm to hear high diastolic
murmur

Procedure, con’t
To interpret heart sounds correctly, you
must clearly identify what sound is S1.
To do this, palpate the carotid artery
while you listen.
 The sound that you hear when you feel
the carotid pulse is S1.
 S2 will follow the pulse

Procedure, con’t

Please see pictures on pages 255-256
of your textbook for approach to
auscultation
Murmurs
They are produced when there is
turbulent blood flow within the heart
 Turbulence may be due to a narrowed
opening of a valve (stenosis) or a valve
that does not close completely, allowing
blood to slosh backwards (regurgitation
or insufficiency)

Describing Murmurs
When in the cardiac cycle do you hear
the murmur? Systole? Diastole? Pansystolic?
 Location (in which of the 4 cardiac
areas do you hear it the loudest?)
 Radiation (does the sound travel
throughout the chest?)
 Duration of the murmur

The Intensity of Murmurs
Grade I = lowest intensity, not heard by
inexperienced listener
 Grade II = low intensity, usually audible
to everyone
 Grade III = medium intensity but no
palpable thrill
 Grade IV = medium intensity with a

thrill
Intensity of murmurs, con’t
Grade V = loudest murmur audible
when stethoscope is on the chest. Has
a thrill
 Grade VI = loudest intensity, audible
when stethoscope is removed from the
chest. Has a thrill

Other Ways to Describe
Murmurs
Pitch (high? Low?)
 Quality (rumbling? blowing? harsh?
musical? scratchy?)
 Is there any relationship to the
respiratory cycle?

Systolic Murmurs
These are ejection murmurs
 May be caused by turbulence across the
aortic or pulmonic valves if they are
stenosed
 May be caused by turbulence across the
mitral or tricuspid valves if they are
incompetent (regurgitant)

Systolic Murmurs, con’t
The murmur falls between S1 and S2
 Sounds like, LUB-shhh-dub

Diastolic Murmurs
Mitral and tricuspid stenosis can cause a
diastolic murmur
 Aortic or pulmonic regurgitation can
cause a diastolic murmur
 Sounds like this: Lub-dub-shhh

Pericardial Friction Rub
These are extra-cardiac sounds of short
duration that have a sound like
scratching on sandpaper
 May result from irritation of the
pericardium from infection,
inflammation, or after open heart
surgery
 Best heard when patient sits and holds
breath

Friction Rub, con’t
A rub that disappears when the patient
holds his breath does NOT come from
the heart. This is probably a pleural
friction rub
 There are three components to a
friction rub…one systolic (during
ejection) and two diastolic (during rapid
filling of the heart and again during
atrial contraction)


Refer to excellent charts regarding Extra
Cardiac Sounds and Murmurs on pages
258-259 in textbook.
Assessment of the Peripheral
Vascular System
Introduction
Peripheral vascular disease - very
common, may involve arteries or veins.
 Arterial diseases include
cerebrovascular, aortoiliac,
femoropopliteal, renal, and aortic
occlusive or aneurysmal disease
 Narrowing of vessels causes a
decreased blood supply, resulting in
ischemia.

Abdominal Aortic Aneurysms
The abdominal aorta is the artery most
frequently involved in the development
of an aneurysm
 Usually occur below the renal arteries
 Few symptoms until it ruptures. You
may discover a pulsatile mass in the
abdomen
 Usually first sign is catastrophic rupture

Microvascular Disease
Diabetes is the most common cause of
microvascular disease
 New recommendations - blood sugar
should be covered with insulin in
hospitalized patients for BG over 150
 Peripheral venous disease often
progresses to venous stasis and
thrombotic disorders (we fear
pulmonary emboli the most)

Review of Symptoms
Pain
This is the principal symptom of
atherosclerosis. Pain is often in calf,
arch of foot, thighs, hips, or buttocks
while walking (“intermittent
claudication”)
 Leriche’s Syndrome…chronic aorto-iliac
obstruction. Pain in buttocks and thigh,
as well as erectile dysfunction

Skin Changes
Color changes are common with
vascular disease
 Chronic arterial insufficiency produces a
cool, pale extremity
 Chronic VENOUS insufficiency produces
a warmer-than-normal extremity (leg
becomes red, erosions develop,
increased pigmentation, swelling,
aching, heaviness

Deep Vein Thrombosis
People with DVT have secondary
inflammation of the tissue around the
vein.
 This produces warmth, redness, and
fever
 Swelling of one leg more than 2 cm at
the ankle or mid-calf should be
considered significant

Edema
Lymphedema results from obstruction
to flow in which there is stasis of lymph
fluid in the tissues
 This produces firm, non-pitting edema
 Seen in women post-mastectomy with
lymph node removal

Ulceration
Persistent ischemia of a limb is
associated with ischemic ulceration and
gangrene
 Ulceration is almost inevitable once the
skin has thickened and circulation is
compromised
 Ulceration can occur with just the
slightest trauma

Ulceration, con’t

Rapidly developing ulcers are commonly
caused by arterial insufficiency, whereas
slowly developing ulcerations are
usually the result of venous
insufficiency
Emboli
Thrombi form from stasis or
hypercoagulability
 Bedrest, CHF, obesity, pregnancy, recent
extended travel on planes, and oral
contraceptives have been associated
with thrombus formation and emboli
 Symptoms depend on where clot lodges

The Physical Examination
Points to Consider in Exam




Inspect for symmetry of extremities
Examine arterial pulses
Auscultate carotid artery with diaphragm
(slightly elevate head on pillow and turn
slightly away from the side being auscultated)
If a bruit is noted, do NOT palpate!
Should not be able to palpate abdominal
pulse unless very thin. Err on side of caution.
Get abdominal ultrasound to R/O aneurysm.
Often too late when bulging mass felt.
Exam, con’t
Palpate abdomen deeply but gently for
a mass with laterally expansive
pulsation (surgical mortality for a nonruptured abdominal aneurysm is only
5%, but rupture increases mortality to
over 90%)
 Listen for bruits over major arteries with
patient lying flat. Listen 2 inches above
umbilicus for presence of aortic bruit

Exam, con’t
Renal artery bruits may be heard about
2 inches above umbilicus and 1-2 inches
laterally from mid-line
 Palpate femoral pulse. The lateral
corners of the pubic hair triangle is
where you will find the pulse. Feel both
femorals so you can judge equality

…more of the exam...
Palpate popliteal pulse…often hard to
feel. Place thumbs on patella and press
remaining fingers of both hands in
popliteal fossa. Have legs in mid-flexed
position
 Palpate dorsalis pedis (top of foot) and
posterior-tibial pulse (inside ankle bone)

Grading Pulses
0 = absent pulse (check with doppler!)
 1+ = diminished
 2+ = normal
 3+ = increased
 4+ = bounding

Capillary Refill
Evaluate capillary refill by compressing
the toe or fingernail tufts until they
blanche.
 Color should return in 3-5 seconds
 Prolonged time for color to return is a
sign of arterial vascular insufficiency

Allen’s Test:
Evaluating arterial supply in arms
Occlude the radial artery by firm
pressure. Ask patient to clinch his fist,
then open the fist and observe the color
of the palm
 Then compress ulnar artery, clinch fist,
and observe color of palm
 Pallor of the palm during compression
of one artery indicates occlusion of the
OTHER artery!

Acute Arterial Occlusion:
The Five P’s
Pain
 Pallor
 Paresthesia
 Paralysis
 Pulselessness

Raynaud’s Disease
Poor peripheral circulation to distal
fingers and toes
 You may see three distinct color
changes: white (pallor) due to
decreased blood supply, blue (cyanosis)
due to increased peripheral extraction
of oxygen, and then red (rubor) due to
the return of blood flow

Diagnostic Tests
Venous doppler flow studies
 Arterial doppler flow studies

CARDIAC LABORATORY TESTS
COMPLETE BLOOD COUNT
(CBC)

WBC
– Increases with inflammation &
phagocytosis



MI
Large hematoma
Pericarditis
– Increases with use of steroids


Treatment of Pericarditis
Treatment of allergic reactions to IV contrast
RBC, HG, HCT, INDICES
Evaluate for anemia as cause of chest
pain, dyspnea
 Evaluate safety for initiation and
continued use of anticoagulant and
antiplatelet therapy

PLATELETS
Evaluate safety for initiation of &
continued use of anticoagulant and
antiplatelet therapy
 Decreases may be due to adverse drug
effect

– Heparin-induced Thrombocytopenia (HIT)
– H-2 blockers (Pepcid, Tagamet, Zantac)
– Aspirin, Plavix
COMPLETE METABOLIC
PROFILE (CMP)
SODIUM (Na)

Increases
– Dehydration
– Increases Na intake

Decreases
– Volume overload
– Decreased Na intake
– Diuretics
POTASSIUM (K)


MUST keep in tight range
Decreases due to:
–
–
–
–
–
–
–
Diuresis
Decreased potassium intake
Diarrhea
Nausea & Vomiting
Gastric Suctioning
Hypoglycemia
Alkalosis
POTASSIUM (K)

Increases due to:
– Renal failure
– Dehydration
– Acidosis
– Hyperglycemia
– Increased potassium intake
– ACE inhibitors
– Hemolysis
HYPOKALEMIA

Often presents as:
– PVC’s
– Atrial tachycardia
– Ventricular tachycardia
– Ventricular fibrillation
– Leg Cramps
HYPERKALEMIA

Often presents
as:
– Bradycardia
– Heart block
– Idioventricular
rhythms
– VTach
– VFib
– Ventricular
arrest
– Muscle
weakness
– Tetany
POTASSIUM

Potassium level should be maintained
4.0 to 5.0 in cardiac patients, especially
with acute MI, Cardiomyopathy, history
of Ventricular arrhythmias, and diuretic
therapy (as long as normal renal
function).
CARBON DIOXIDE
Measures bicarbonate level of blood
 Measures metabolic state

BLOOD UREA NITROGEN
(BUN)

Increased level (azotemia) with
impaired renal function caused by:
– CHF, Dehydration, Shock, Stress, Acute MI

Increased levels also with renal disease
and GI bleed
CREATININE (CR)

Increased level indicates worsening
renal function
GLUCOSE (BG)
 May
elevate with stress such
as with MI
LIVER FUNCTION TESTS
AST, ALT, Alkaline Phosphatase
 May elevate in CHF due to hepatic
congestion
 Will elevate in low perfusion states
causing “shock liver” due to ischemia.
Common with cardiac arrest S/P
resuscitation, prolonged hypotension,
shock states, embolic event.

Liver Function Tests

May elevate due to anti-lipidemic drugs.
Usually not a problem unless 2X normal
range.
MISCELLANEOUS LABS

Amylase & Lipase
– Increases with pancreatitis or GB disease
– May order if suspect GI source of chest
pain

Magnesium
– Decreased levels cause arrhythmias
– Always check in atrial & ventricular
arrhythmias and QT prolongation
MISCELLANEOUS

Thyroid Function Tests
– Thyroid abnormalities can cause:



Arrhythmias
Fatique
Anemia
– Usually start by checking TSH. If
abnormal, check full thyroid panel
CARDIAC ISOENZYMES

Total CK (Creatine Kinase)
– Enzyme found in heart, skeletal, and brain
muscle cells. Enzyme is released with
injury to cells
– Increases with acute MI, myocarditis, postCABG, cardioversion(defibrillation)
– Can also elevate with rhabdomyolysis. May
see with cocaine intoxication & adverse
effect from statin drugs for
hypercholestolemia
CARDIAC ISOENZYMES

CK-MB
– Specific to myocardium
– Increases with acute MI, myocarditis ,
post-CABG, cardioversion
– May also elevate with chronic renal failure
– With acute MI, MB occurs in serum in 6-12
hrs. & remains for 18-32 hrs.
– Presence is diagnostic of MI
CARDIAC ISOENZYMES

MB Index
– Percentage of MB in comparison with total
CK

*** Three sets of cardiac isoenzymes
should be ordered 8 hrs. apart to
diagnose/confirm acute MI.
TROPONIN I and T
Troponin I more specific
 Unique to heart muscle
 Released with very small amounts of
damage as early as 1-3 hrs. after injury
 Peaks in 12-48 hrs.
 Levels return to normal in 7-10 days.
 Useful in delayed diagnosis of MI also

TROPONIN T
 May
also elevate in unstable
angina, myocarditis, chronic
renal failure, acute muscle
trauma, rhabdomyolysis,
polymyositis, and
dermatomyosis.
MYOGLOBIN
Oxygen-binding protein of striated
muscle. Released with injury to muscle.
 Used as early marker of muscle damage
in MI
 Elevates in 2-4 hrs.
 Peaks in 8-10 hrs.
 Returns to normal in 24 hrs.

B-type NATRIURETIC PEPTIDE
(BNP)
Hormone produced by ventricles of the
heart that increases in response to
ventricular volume expansion and
pressure overload.
 Marker of ventricular systolic and
diastolic dysfunction
 Useful in diagnosing CHF
 Normal is less than 100 ng/L

CARDIAC DIAGNOSTIC TESTS
ELECTROCARDIOGRAM
(EKG or ECG)
Cardiac rhythm
 Chamber enlargement
 Conduction abnormalities
 Electrolyte and toxic disorders

– Peaked T-waves = Hyperkalemia
– U waves = Hypokalemia
– QT prolongation = toxic drug effects
EKG cont.

Acute MI
– T wave inversion = ischemia
– ST elevation = acute injury
– Q waves = Transmural MI
– CAN HAVE AN MI WITH NORMAL EKG!!
– Cannot read with Left Bundle Branch Block
CHEST X-RAY (CXR)
Heart size
 Calcification on valves and arteries
 Evidence of CHF

– Pulmonary vascular congestion
– Pleural effusions

Masses
ECHOCARDIOGRAM
(ECHO)

Structural Abnormalities
– Anatomical
– Presence of thrombi, vegetations,
– Presence of pericardial effusion/tamponade
Chamber sizes
 Valvular function
 Left ventricular function

– Wall motion, Ejection Fraction (EF)
TYPES OF ECHOCARDIOGRAM

TRANSTHORACIC (TTE)
– Most common

Transesophageal (TEE)
– Usually ordered to evaluate for
vegetations, valvular disorders, and
thrombi.
STRESS TESTING


Exercise Treadmill testing
Myocardial Perfusion Imaging (MPI)
– Often called misnomer, Thallium scan
– Types – Exercise, Persantine, Adenosine,
Dobutamine

Stress Echocardiogram
– Types – Exercise, Dobutamine

All done to evaluate for myocardial ischemia
RADIONUCLIDE ANGIOGRAPHY
Often called MUGA scan – stands for
multiple gated angiography
 Determines ejection fraction
 Almost always automatically done with
MPI now

COMPUTED TOMOGRAPHY
(CT)

Helical CT
– Uses IV Contrast
– Used to diagnose Aortic dissection,
Pulmonary emboli

Plain CT
– Abnormal masses (with or without
contrast)
– Hematoma or retroperitoneal bleed –
better with IV contrast
CT cont.

Ultrafast CT
– No contrast used
– Detection of coronary artery calcification as
indicator of atherosclerosis
– The higher the score, the more calcium
detected
CARDIAC CATHETERIZATION
Uses IV contrast
 Reveals:

– Pressures in chambers/Aorta
– LV wall motion and ejection fraction
– Visualization of coronary anatomy
– Valvular function
ARRHYTHMIA MONITORING
Telemetry
 Holter monitor – continuous recording
of heart rhythm, usually for 24 hrs.
 Event recorder – records specific events
to correlate symptoms with possible
arrhythmia, worn for several weeks
 Loop recorder – implanted in chest wall,
continuous recording, then explanted.

ELECTROPHYSIOLOGY STUDY
(EPS)
 Evaluation
of conduction system
 Inducibility of arrhythmias
 Effectiveness of Antiarrythmic
therapies
Ventilation-Perfusion Scan
(VQ Scan)
 Used
to diagnose Pulmonary
embolism
 Will read as high, moderate, or
low probability for PE