OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE

Exam 1 | Dr. Donato Maraon | September 24, 2012
OUTLINE
Common Cardiac Symptomatology
A.
Chest Pain
1. Attributes of Pain
2. Definitions
3. Chronic Recurrent Chest Pain Syndrome
4. Acute Chest Pain Syndrome
5. Case Discussion

B.
Dyspnea
C.
Palpitations
D. Edema
E.
Cyanosis
F.
Syncope
II. Importance of History and PE

The lecture is similar from block Bs Lecture but we changed the formatting though kasing ang gulo nung topic. So if
mas naguluhan kayo sorry.
Some changes:
1. All the symptomatology are now under common cardiac symptomatology.
2. Differentials for chest pain have been divided into chronic and acute.
I. COMMON CARDIAC SYMPTOMATOLOGY

Symptoms: complaints of the patient (most common complaint: pain); Includes chest pain, dyspnea,
palpitations, edema, cyanosis, syncope

Signs: doctors objective findings and observations

A. CHEST PAIN

Chest pain: most common but not exhaustive - can be caused by other factors such as hypertension

ATTRIBUTES OF PAIN (PPQRSTO)

Provocative what provokes/triggers the pain

o

Is it precipitated by effort (exertional)?

At what time does it appear? When you are trying to get up, moving the body, etc

Palliative what relieves/palliates the pain

Medications, therapy, etc

Quality the nature of the pain

Sharp, burning, pricking, stabbing, strangulating, oppressing, ache similar to muscle ache, etc.

Region/Radiation location (primary region where the pain is felt), central region, how wide the coverage is
and where the pain radiates or is worst
o

Central precordial pain where does it radiate? Back? Leg?

Hard to interview Filipinos doon, diyan vague descriptions of location

Severity intensity: mild, moderate, severe

o

May use a scale from 0 to 10 (worst)

Give open-ended questions

Timing
o

Onset abrupt, worse at start, insidious, builds up/gradual

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Duration how long does it last: few seconds, minutes, hours

Frequency once every month, once every 2 years, etc.; avoid using phrases such as rarely,

o
sometimes

Other associated symptoms important to be able to identify the etiology

o

Nausea and vomiting, cold sweats, palpitations, co-morbidities and other risk factors, etc.

Always observe while you are examining (these might give you clues on the symptoms of the patient)

DEFINITIONS
From 2015 Block B:

Spontaneous: comes and goes, not related to effort

Rest: pain gradually subsides when the effort is eliminated

Nitrates: coronary vasodilators; this as a palliative factor is characteristic of myocardial ischemia.

Fastest acting- sublingual nitrates

Diffuse: not more than one fingerbreadth

Time: anything exceeding 20 minutes is associated with myocardial infarction

Severe: acute coronary syndrome

CHRONIC RECURRENT CHEST PAIN SYNDROME

DDX
1. CARDIAC ETIOLOGY: Classic AnginaA

Fixed arterial stenosis causing symptoms, usually while exerting self

o

Quality of chest pain of aortic stenosis is the same as that of angina

Imbalance in myocardial oxygen demand outstripping the supply

In anemics, the same amount of oxygen will be distributed to the tissues as normal if there is increase in
Cardiac Output or if there is increase in Oxygen Extraction Rate in the tissues.
American Heart Association (AHA): "a medical term for chest pain or discomfort due to coronary heart

o
disease."
o

Chronic angina- myocardial ischemia

Nocturnal angina- provoked during sleep

2014: chest pain due to temporary myocardial ischemia, usually secondary to coronary atherosclerosis

2014 trans: Less than 15-20 minutes unstable coronary syndrome, if greater than 30 minutes, acute

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
2. CARDIAC ETIOLOGY: Atypical Angina/Angina PectorisA

the chest discomfort of myocardial ischemia is a visceral discomfort that is usually described as a heaviness,
pressure, or squeezing (Harrisons 17th Edition page 87).
While at rest or while having atypical workload

Table 1. Differentiating the quality of angina

TYPICAL
FEATURES

ATYPICAL
FEATURES

DIABETICS

Heaviness
(vague ache in
the chest)
Squeezing
Constricting
Strangling
builds up
over time

Burning
Stabbing
Pin Pricking

May have
paresthesia/
change in
sensorium, will
describe things
differently

Coronary Artery Diseases (CAD)

most common etiology for coronary insufficiency

common
symptom
IS
ANGINA.
ANGINA
(http://www.nhlbi.nih.gov/health/health-topics/topics/angina/)

The aforementioned features are usually the basis for the determination of typical or atypical angina. In some
references this is based on three classic signs:

is

symptom

not

disease!

(1) substernal chest discomfort with a characteristic quality pressure /squeezing/heaviness an

o
duration
o

(2) provoked by exertion or emotional stress

(3) relieved by rest or nitroglycerin.

Typical angina if it has all these three signs and atypical if it has two.

Angina symptoms resemble those of a heart attack. However, angina symptoms usually last only one to
five minutes, while chest pain from a heart attack may last for hours. Angina symptoms normally diminish after
resting or taking angina medications. Heart attack symptoms do not improve with rest, and angina medication will
not reduce heart attack chest pain

Angina (definition) chest pain caused by restricted blood flow to the heart (called ischemia). It often occurs
when you are under emotional or physical stress, such as exercise. When the heart doesn't get enough oxygen from
the coronary arteries, you feel a squeezing chest pain or pressure across your chest that usually goes away after you
stop the activity. The most common cause of angina is hardening of the arteries (atherosclerosis). (www.umm.edu)
Usual Distribution of Myocardial Ischemia

Retrosternal chest pain

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012

Central chest radiates to neck and jaw (angina dentis- dental pain); more commonly down the left arm
(following dermatomal distribution)

Can also radiate to right arm (for right coronary problems), epigastrium, or back.

Dermatomal origin of heart involved (hence different areas of referred pain

Tooth Ache and throat ache can also be a sign of MI up to the neck and into the jaw.

Figure 1. Usual Distribution of ischemic chest pain: dermatomal distribution of the heart
*epigastrium: may suggest right coronary artery involvement
3. CARDIAC ETIOLOGY: Mitral Valve Prolapse

An abnormal systolic ballooning of part of the mitral valve into the left atrium, resulting in a floppy leaky valve.
o

Younger patients usually have this instead of coronary insufficiency

Usually stays as it is, without hemodynamic deterioration of the valve or stroke

2-5% of people, especially the females commonly seen in the clinics

Not very life threatening, but is associated with mitral regurgitation in the United States.

Table 2. Chronic Recurrent Chest Pain Syndromes: Cardiac Differentials*

Atypical Angina should be
Mitral Valve Prolapse
Classic Angina
distinguished from nonaffects 5% of females
cardiac chest pain**
During effort/ exertion(e.g.
Spontaneous/cold
Spontaneous
walking or during very hot or
weather(mechanism is
very cold weather); due to
vasocontriction/ coronary
demand for oxygen (demand
vasospasm = supply type of
P
type)
angina rather than demand type),
pain at night

Rest / nitrates(diagnostic if chest

pain goes away in a few minutes)

Nitrates

Variable (TYPICAL: Squeezing,

constricting, pin pricking,
stabbing tightness, pressure,
heaviness, strangling,vague
chest discomfort)
basta mabigat
SEVERE: parang may hollow
blocks sa chest

Variable(burning, pricking,
stabbing pain; found in diabetics
and the elderly; itis not life
threatening)

Ian, Aca, Hannah

Spontaneous (can be
incapacitatingneed to use a Bblocker)
Variable(diagnosis is based on
echocardiography)

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Classic Angina
R

Retrosternal/ precordial(diffuse
pain, more centrallylocated)
Mild to moderate*** (stable =
same level of intensity for some
time now)
1-30 min
Typically <15-20 mins
If > 20 mins. = Myocardial
Infarction (MI)
Risk factors (i.e. Age: M>55/45*,
F>65/55*, 5 most common risk
factors: Smoking, DM,
hypertension, dyslipidemia,
genetic predisposition)
Associated factors: obesity,
stress

Atypical Angina should be

distinguished from noncardiac chest pain**
Retrosternal (not typical ; maybe
different in location); especially
with diabetics, they usually
present with atypical angina
Mild to moderate

Mitral Valve Prolapse

affects 5% of females
Left anterior, variable(can be
under the breast)
Mild severe(not life threatening
but pain is incapacitating)

1-30 mins
Maybe 2-3 mins

Mins hours

Also w/ CSAP
(Chronic Stable Angina Pectoris;
higher risk in diabetic patients
and in women, presence of at
least 1 risk factor for coronary
disease)

Young female(oftentimes the

complication is benign)

*These are just common diseases (other diseases may present with similar pain/symptoms)
**We should not dismiss the complaint just because it is atypical
***The Canadian Cardiovascular Society (CCS) grading of angina pectoris was described in the medical literature in
1976. This grading system of the severity of effort angina has been accepted throughout the world over the past 30
years.
Table 3. Canadian Cardiovascular Society Grading of Angina Pectoris
Grade
Description
Grade I

Ordinary physical activity does not cause angi

na, such as walking and climbing stairs. Angi
na with strenuous or rapid or prolonged
exertion at work or recreation. (least
bothersome)

Grade I
I

Slight limitation of ordinary activity. Walking

or climbing stairs rapidly, walking uphill,
walking or stair climbing after meals, or in
cold, or in wind, or under emotional stress, or
only during the few hours after awakening.
Walking more than two blocks on the level
and climbing more than one flight of ordinary
stairs at a normal pace and in normal
conditions (provoked by more than usual to
usual activities)

Grade I
II

Marked limitation of ordinary physical activity.

Walking
one or two blocks on the level and climbing o
ne flight of stairs in normal conditions and at
normal pace (provoked by less than usual
activities)

Grade I
V

Inability to carry on any physical activity with

out discomfort,
anginal syndrome may be present at rest (dis
abling or severe, pain at rest)

References:Campeau Lucien. Grading of angina pectoris. Circulation 197654:5223 http://www.ccs.ca/download/position_statements/

Grading%20of%20Angina.pdf

4. GI ETIOLOGY: ESOPHAGEAL, GASTRIC, BILIARY

Table 4. Chronic Recurrent Chest Pain Syndromes: GI differentials

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012

Esophageal

Gastric

Biliary

Acid Reflux Disease

Gastric/Peptic Ulcer

Gallbladder stones

Feed (a common provoking factor), exercise,

supine/lying down after a meal (due to reflux;
especially if patient has hiatal hernia or weak
GI sphincter; Gastroesophageal reflux:
HEARTBURN)
Drinking, proton pump inhibitors, antacids,
burping,(H2 blocker/proton pump inhibitors
decrease acidity of gastric secretions) pain
is due to acid going back to the esophagus,
SLN

Fasting(or 2hrs after eating);

e.g. peptic ulcer

Feeding (precipitated
by high fat meals;
spastic)

Feeding, Rx (antacids: H2
blockers, proton pump
inhibitors)

Spontaneous,Rx(antis
pasmodics,
antiparasympathomim
etic agents)

Variable (burning, lower part of the chest;

angina-like)

Variable (hunger- like pain;

gnawing pain/discomfort)

Colicky, crampy or
spastic/painful

Substernal(may radiate to the epigastrium;

visceral ache)

Epigastrium/ lower sternum

Right upper quadrant

but can radiate to
chest and shoulder

Mild - severe

Mild moderate; severe(may

imply persistence of a
perforation if severe)

Mild, severe

5-60 min
earlier)

Hours(1.5 hrs or longer after a

meal; antacids for immediate
relief)

Min-hrs

Angina-like(esophageal spasms also

manifested but not relieved by nitrates)

Epigastric pain

4 Fs (risk factors of
gallstones: fat,
female, fertile, forty),
nausea and vomiting

(usually not relieved

Your notes here:

5. OTHER ETIOLOGY: PLEURAL, MSK, FUNCTIONAL

Table 5. Chronic Recurrent Chest Pain Syndromes: Other differentials
Pleural (more diffuse) or
Musculoskeletal (felt almost by
Pulmonary (acute pericarditis,
everyone unless sedentary)
pneumonia)
P

Respiration (deep breaths);

coughing; pleural
inflammation(acute pleuritis,
asthma)

Analgesics (anti-inflammatory,
narcotics)

Variable (sharp, more localized

pain)

Variable (wherever pathology

is, esp. Left/ Right chest, back)
Mild severe (unequal
breathing; leaning on one side
to protect the hurting area
dependent if acute)
Variable(until inflammation
abates)
Cough & fever (because
inflammation involved), cough
associated pain

T
O

Ian, Aca, Hannah

Change in Position, upon

application of pressure, upon
motion; elicit tenderness; may be
recurrent; may also be associated
with cough
Rest, Rx (analgesics and/or nonsteroidals because its an
inflammation)
Variable
(dull muscle type
pain, depends on position and
motion)
Variable

Functional* (psychosomatic)

Supratentorial; Stress: all in the

head no organic basis;
psychiatric (especially Borderline
Personality)
Relaxation; psychiatric intervention;
extensive workup; deliberate thought
on diagnosisreally depends on
history
Variable (but can be distressing
especially if unknown etiology)
Substernal

Mild severe

Mild severe

Variable

Hours

Tietzes Syndrome acute

costochondritis; inflammation of
costal cartilages (costochondral
and sternocostal junction),
tenderness and sharp localized

Da Costas(soldiers heart) most

severe; in soldiers sent to war
patient with profound psycho
somatizations (loss of motivation,
energy lack, chest pains, vague

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Pleural (more diffuse) or
Pulmonary (acute pericarditis,
pneumonia)

Musculoskeletal (felt almost by

everyone unless sedentary)

Functional* (psychosomatic)

pain (a few points in the chest)

symptoms)
- more common in females beyond -may require psychiatric care;
forty; PE evoke tenderness by
circulatory neurastemia
touching chest pain
*Functional aka supratentorial (its all in the mind): but its symptoms is as real as those with organic symptoms
Your notes here:

Table 6. Chronic Recurrent Chest Pain Syndromes: Summary

Differential
Provocative
Palliative

Other

Angina

During effort

Rest, sublingual nitrates

Mins

Coronary disease
risk factors

Esophageal

Feeding, exercise,
supine position

Burping, drinking, SLN

Mins

Angina like

GI

Fasting

Food, Antacids

Mins

Epigastric pain

Biliary

Feeding

Spontaneous, Rx

Mins

Crampy, colicky

Pleural, Pulmonary

Respiration, cough

Analgesics

Var.

Assoc.
with cough and
fever

Musculo-skeletal

Position, motion,
pressure

Analgesics, (muscle
relaxants)

Var.

Tietzes syndrome

Functional

Stress

Relaxation

Var.

Da Costas
syndrome

Few modern doctors are equipped to recognize the subtle cases of angina, largely because they are ignorant of these
details or unwilling to invest time in history takingOf the million coronary angiograms done in 1993, 200,000
revealed normal coronary arteriesHad Levines teachings been heeded, few if any of the patients would have been
subjected
to
such
a
costly
and
invasive
procedure
Frequent reliance on a so-called work-upIs testimony to lack of clinical skills
-Bernard Lown, MD (1985 Nobel Peace Prize)
Point of Emphasis: History and PE matter.
ACUTE CHEST PAIN SYNDROME DDX
Table 7. Acute Chest Pain Syndromes
Common
Clinical Clues
Causes
ACS: Acute
MI*
ACS:
Unstable
Angina*
Acute
Pulmonary
Embolism*
Dissecting
aortic
aneurysm*

Prior angina, risk factors,

>20minutes, crescendo

Dyspnea, clear lung fields (this is not

a pulmonary problem, its a vascular
problem), Deep Vein Thrombosis is a
risk factors
Unequal phases- radial, brachial,
femoral
You can hear regurgitations

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Common
Causes

Clinical Clues

Acute
Pericarditis

Pleuritic (aggravated when leaning

forward or taking deep breaths),
central chest, anterior friction rub

Acute
Pneumonia

Pleuritic, cough
After alcohol,
gnawing

Acute Gastritis
Acute
Pancreatitis

Nausea and
vomiting

Acute
Cholecystitis
Acute visceral
problems
(abdomen)

After alcohol,
gallstones
Jaundice

Nausea, vomiting, cold sweat

*Three diseases associated with chest pain that would require immediate attention (life threatening). These Big
Three diseases can be ruled out by CV angiogram (however relying on this test can make your mental capacities
deteriorate (Maranon, 2011; basing from Lown)
**Acute Coronary Syndrome (ACS): Acute MI and Unstable Angina. Unstable Angina is without necrosis (thus is
diagnosed after MI is ruled out)
***Sometimes nausea and vomiting together with diffused pain can be a manifestation of acute MI (respect these
symptoms!)

Fixed obstruction kind can result to unstable angina.

o

Intensity

Frequency

What provokes it

Acute coronary syndrome results from plaque rupture

o

Necrosis is present in acute MI. Acute thrombosis occurs.

Diagnostic of necrosis: Enzymes.

Acute MI is ruled out if there is no evidence of myocardial necrosis, negative for EKG changes, and no
characteristic pain. If enzyme tests negative, then it is unstable angina.
Lethal

Acute MI, Unstable Angina, Acute Pulmonary Embolism, Dissecting Aortic Aneurysm
Unstable Angina

more severe, more frequent, needs ICU confinement; crescendo angina (increasing intensity/
worsening pattern, unlike in classic and atypical angina), must monitor angina within the first month because it
can head south to this
Dissecting Aortic Aneurysm

aorta tears; aortic insufficiency murmurs are heard on PE; the pain is more severe at the outset and it
radiates to the back and the butt (depending on the extent of the aneurysm)

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
o

patients feel like theyre going to die (20% die at initial pain); unequal pulses depending on the levels
of compromise of aortic branches
Proximal aortic dissection

manifests as chest pain

Acute pulmonary embolism

shortness of breath, clear lung fields (a problem of perfusion, not ventilation), oxygen desaturation/
hypoxemia, pleuritic, pulmonary hypertension- related, RV cannot compensate: Right heart failure. Pneumonia=
crackles,
Acute pericarditis- pericardial rub
Acute pneumonia
febrile

episode

with

pleuritic

pain;

inspiratory

pleuritic

rub

CASE DISCUSSION
Case 2

The pain usuallyCase

occurs
1
The patient is a 40F with
during exertion but
pain Do
on exertion,

In chest
this case:
not use endoscopy unless the patient does
sometimes at rest or after
usually after washing
not
respond
to
medications/
treatment
fatty meals. It is relieved
clothes
by nitrates or rest or
sometimes
by belching
Diagno
Upper extremity effort (musculoskeletal
sis pain); can also be due to angina BUT the
Diagno multiple etiologies: biliary, esophageal,
type of effort is important.
B. DYSPNEA
sis atypical angina (Be open minded of other

Definition:
The patient
possible etiologies. Do not Caveat
be limitedInto
angina, effort
as light as walking
can is not necessarily in distress but is
shortness
of breath
what is being discussed. )
cause the pain. suffering
The kind from
of effort
will
characterize the pain.
TWO MAIN
TYPES of
OFparsimony:
DYSPNEA:simplest
CARDIAC
Caveat
The concept
wayAND
to
PULMONARY
explain (only one disease)
Table 8. Differentiating cardiac and pulmonary dyspnea
Cardiac
Pulmonary
Usually from congestive heart failure or
Obstructive pulmonary airway
angina, but these do not include edema
syndromes, e.g. asthma
Progressive and occurs on exertion
Progressive (chronic: COPD or end stage
lung disease)
Progressive: takes more effort at the outset,
On exertion
then less and less in time until it occurs at
episodic (bronchial asthma, which has
rest
reversible, intermittent causes)
2015: RHD, MI or cardiomegaly
Late
Immediate, can happen earlier on
Orthopnea
unless in cases of acute mitral valve
regurgitation
Relieved by sitting orstanding
Expectorate:
relieved by sputum production & cough
PND** (Paroxysmal reduction of central venous pooling
Nocturnal Dyspnea) 2015: when patient is supine, there is
2015:expectorating phlegm, blood
Cardiac Asthma
pulmonary congestion due to increased
blood flow to the lungs
Cough
Late symptom
Early prominent symptom
Ascending (from the feet up)
Ascending(only in a R-sided failure or RV
Edema
Biventricular- from Left heart failure (CAD)
heart failure from pulmonary
hypertension core pulmonare)
*To differentiate the different forms of dyspnea, be detailed as possible, since symptoms are similar for both the
cardiac and pulmonary types
OTHER TYPES OF DYSPNEA SYNDROMES
Orthopnea - dyspnea when in supine; difficulty breathing in supine position, late sign
Paroxymal nocturnal dyspnea** - episodes of sudden dyspnea and orthopnea that awaken the patient from sleep,
usually one or two hours after going to bed, when you sleep, get up and youre out of breath
Trepopnea dyspnea when lying on side/lateral decubitus position, can occur due to heart failure or pulmonary
conditions or disease states

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Platypnea dyspnea when upright usually due to a diaphragmatic problem; differentials: hepatopulmonary syndrome
due to pulmonary shunting, diaphragmatic mismatch
Treponea and Platypnea are issues with changing perfusion-ventilation ratios and congenital diaphragm problems
Non cardiac causes of dyspnea: Dyspnea may be caused by severe anemia and hypoxia, which are not exclusively
cardiac or pulmonary causes
Caveat
Case 1
Diagnos
is
Caveat

Case 2

Diagnos
is
Caveat

Doc, madali po akong mapagod

easy fatigue vs. exertional dyspnea
difference in vernacular: tire easily (easy
fatigue) versus out of breath (exertional
dyspnea)
Differentiate between pathologic and
physiologic
Easy fatigue: effort intolerance due to
low cardiac output
Exertionaldyspnea: congestive heart
failure
Pathologic if the symptom is not age/
appropriate
Doc, hinihingal po ako kahit walang
ginagawa, saka mayroon ho akong kaba,
nahihilo ako, at nanlalamig, at lagi akong
hinang-hina
hyperventilation syndrome
The case may appear non-specific but
these signs are characteristic of
hyperventilation syndrome, which may be
a normal thing and would require patient
to blow into rebreathing bag

Dyspnea may be normal or abnormal depending upon the situation. Therefore, we need to elicit more information from
the patient during the history taking. Remember that cardiac and pulmonary symptoms may always be
present on exertion, orthopnea, PND, cough, and edema. Proper diagnosis entails a good history taking which
involves the clear characterization of the symptoms and correct understanding of the patients descritption of cardiopulmonary symptoms.
C. PALPITATION
Definition: Awareness/sensation of ones heartbeat
Can be:
o Singlet (skipped beats)
o Rapid succession of palpitations (tachyarrhythmia)
o How to differentiate? Ask the patient to tap on the table following the rhythm of his/her perceived heartbeat
Can develop during exercise
Not always tachycardia or bradycardia
Table 9. Differentiating functional and organic palpitations
Functional
Start
Gradual
End
Gradual
Trigger
Stress
Rate
<<100

Other Symptoms

Organic/ Pathologic
Sudden
Sudden
None
>>100 (they can have
supraventricular or ventricular
tachycardias occurring and
because of that, extremely rapid
rate)

Anxiety (a little bit of tremulousness, stage fright)

* Many complain about this!

2015: although there are some

bradycardic palpitations)
Chest tightness, shortness of
breath, syncope

Caveat
Case 1
Diagno
sis

Doc, lagi po akong kinakabahan

You can only come to a diagnosis if you ask the
patient further. Ask: Ano pong ibig niyong sabiing
kinakabahan?[Do not suggest an answer. If you

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Caveat

are prone to suggest, give multiple choices.

Let the patient explain what s/he means

D. GENERALIZED EDEMA
characterized by an (abnormal) accumulation of water (actually an accumulationof salt, whichbringswaterwith it)
generally PAINLESS
Table 10. Differentiating the different types of edema
Cause
Description
Renal
Descending

Hypoalbuminic states: puffy eyelids (periorbital edema) and face,

especially in nephrotic syndrome

Hypervolemia, acute renal failure

Two types: Acute renal failure and nephrotic syndrome

Hepatic, systemic
Centrifugal

Starts in the abdomen (ascites) due to portal hypertension

As secondary compensatory mechanism, you get it in your feet

next
Cardiac and Pulmonary
Ascending
(Dependent edema)

Feet first, bilateral then upward, may evolve to anasarca

(generalized edema)

Heart failure (L&R for cardiac, R sided for pulmonary)

Caveat
Case 1
Diagno
sis
Caveat

This 74F has been having bilateral ankle swelling

for the past month, she can hardly walk
Ankle Arthritis
Check first if there is pain since arthritis and gout
are usually painful. Edema is painless.

E. CYANOSIS
Definition: bluish color of the skin and mucous membranes resulting from an increased quantity of reduced
hemoglobin (i.e., deoxygenated hemoglobin) or of hemoglobin derivatives (e.g., methemoglobin or sulfhemoglobin)
in the small blood vessels of those tissues. (Harrisons 18 thed)
Common locations: in the mucous membranes (of the mouth), nail beds, conjunctivae
Pathophysiology:
o Increase in the quantity of venous blood as a result of dilation of the venules and venous ends of the capillaries
~OR~
o Reduction in the saturation of arterial blood (SaO2) in the capillary blood
o Leads to increase in the quantity of reduced hemoglobin in mucocutaneous vessels
Cyanosis becomes apparent when concencentrations of reduced hemoglobin in capillary blood exceeds 40g/L (4g/dL)
At least 5 grams per cell or greater (of desaturation):
o It is the absolute, rather than the relative, quantity of reduced hemoglobin that is important in producing
cyanosis (Harrisons, 18th ed)
Thus, cyanosis is more appreciated in a polycythemic person rather than an anemic person
Anemic patient w hemoglobin at 8, O2 saturation of 75% due to pulmonary disease desaturation is of 8 = 2
not cyanotic because degree of deoxyhemoglobin is only 2
o Patient with hemoglobin of 16, 75% saturated or 4 is not yet cyanotic (you need more desaturation for
cyanosis to manifest)
It is easier to see desaturation or cyanosis
o In a polycythemic person
o In fair skinned people than dark skinned (skin color matters)
o Better detected in nail beds and malar prominences in fairer skinned persons
o In mucous membranes than nail beds

Table 11. DeoxyHb Concentration that cause Cyanosis

DeoxyHb
Concentration
Normal
5 g/dl
Met Hbanemia (Abnormal Hb)
1.5 g/dl
*congenital or acquired, from abnormal Hg or drugs (nitrates)
*usually in toxic concentrations and hemoglobinopathies
Sulf Hb (Abnormal Hb)
0.5 g/dl
Met-Hb and Sulf-Hb arise from hemoglobin congenital problems and toxicities (nitrate poisoning)
Can be congenital or acquired
PATTERNS OF CYANOSIS: CENTRAL OR
PERIPHERAL
Table 12. Differentiating central and peripheral cyanosis
Central
Peripheral

Ian, Aca, Hannah

UPCM 2016A: XVI, Walang

Kapantay!

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Sirs words:
Desaturated centrally
O2 saturation is low due
to a cardiac pulmonary
condition
The arterial blood has low
oxygen level (hypoxemia
leading to arterial
oxygendesaturation from
the aortadeoxyhemoglobin).
Cyanosis is observed both
in mucous membranes
(mouth, lips, palpebral
conjunctiva and
especially under the
tongue) and nailbeds
Happens with congenital
heart disease, heart
failure, pulmonary edema

Sirs words:
Caused by something
in the periphery
(vasoconstriction, cold
weather)
There is
vasoconstriction
(demonstrated by
touching ice), arterial
venous occlusions,
hemostasis and arterial
blood has normal
oxygen level (normal
saturation)
But for some reason,
cutaneous blood flow
slows down and
decreases, and the
tissues extract more
oxygen from the blood
There is an increase in
venous deoxygenated
blood in the capillaries,
and only the nailbeds
are cyanotic

This phenomenon can be attributed to:

Vasospasm (Raynauds phenomenon- characterized by the focal vasoconstricted state of the
arteries), ex. Digital arteries

A thrombus, embolus or a normal response to a cold environment or anxiety

It could also be PDA: Patent Ductus Arteriosus wherein the deoxygenated blood flows to the lower
extremities (only the lower extremities are cyanotic, the upper extremities and oral mucosa look normal)
Polycythemic (with Hb<20) get cyanotic earlier than anemic.

Caveat
Case 1

The toes were cyanotic but her fingers

were not
Diagn Differential cyanosis from PDA
osis Reverse PDA
There is a right to left shunting of blood
past the subclavian artery, and the
upper extremities are spared
Note that PDA is a left to right shunt
Review: Patent Ductus Arteriosus
Ductus Arteriosus: Communication between the aorta and the pulmonary artery ligamentum arteriosum
Patent DA: The ductus arteriosus still persists as a vessel leading from the bifurcation of the pulmonary artery to the
aorta just distal to the left subclavian artery instead of closing after birth
In adult patients with PDA, pulmonary pressures are normal and a gradient and shunt from aorta to pulmonary artery
persist throughout the cardiac cycle.
Pulmonary pressure is 1/6 of the systemic circulation. Blood from the left heart goes upward (fingers), mixed blood
goes downward (feet).
Differential cyanosis from PDA
o May be due to preferential shunting of blood to the feet via the patent ductus arteriosus (PDA).
o Differential diagnosis include:

Diabetes and Eisenmenger syndrome- patients with a large communication between the two circulations at
the aortopulmonary, ventricular or atrial levels and directional or predominantly right to left shunts because of
high resistance and obstructive pulmonary hypertension

Severe pulmonary vascular disease results in reversal of flow through the ductus, unoxygenated blood is
shunted to the descending aorta, and the toes, but not the fingers, become cyanotic and clubbed termed
differential cyanosis.
F. SYNCOPE
Syncope is the relatively abrupt loss of consciousness(2015: brief, seconds to a few minutes and due to decreased
blood flow in the brain), with or without a short prodrome.
Presyncope dizziness
Some people develop syncope after dizziness
Doc nahihilo akowhat type? Characterize and describe!
Table
13. Types
of Dizziness
Ian, Aca,
Hannah

UPCM 2016A: XVI, Walang

Kapantay!

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Vertigo

Disequilibrium

sensation
of
spinning
or the
room is
spinning

Syncope/ Near
Syncope
less than vertigo,
passing out
may be ear problems/ (2015: near
vestibular or the CNS/ faintness, about
central connections in to pass out,
the brain (2015:
light
sense of imbalance;
headedness),
mild kind of vertigo;
metabolic
problem with
sometimes
proprioceptors,
(hypoglycemia
stereognosis;
but thats not
unsteady gait)
our topic since
this is cardio)
Stokes Adams

Types and causes of cardiogenic syncope

Stokes-Adams/ cardiac (syncope)- sudden cessation of

cardiac function and effective CO, complete heart block;
bradycardia(from complete heart block)causing loss of
consciousness
Vasovagal/Common
faintaka
neurocardiogenic
syncope(2015: Neurologic cause with prodrome(flashes of
light, weakness and cold clammy sweat), more benign;
interaction of cardiac mechanoreceptors as well as paraand sympathetic receptors; vasodepressor or inhibitor. Can
be prevented because there are warning signs)

Table 14. Qualities of syncope

Vasovagal(the common faint e.g. in the heat)

Onset

Sudden

With short prodrome (stomachache, dimming of vision,

lightheadedness); close to hyperventilation; position
dependent, aka common faint

End

Asymptomatic, (2015: no post ictus,

pt has no memory of occurrence)

Usually no post ictus (post seizure) except for a few

brief jerks sometimes

Duration

Seconds (or else the patient will be

dead)

Minutes to hours, relieved by lying down (blood goes

to head)

Table 15. Other Causes of Syncope-like Episodes (DDx)

Absence seizures
Situational(2015: preand post-ictal stages,
weak and sleepy upon
revival, non convulsive
seizures)
Cough syncope
Situational (2015: benign
and common in elderly,
loss of consciousness
after coughing bout due
to increased vagal
stimulation)
Post micturition
Situational (2015: benign
syndrome
and common in elderly,
pt is woken up by an urge
to urinate and losses
consciousness upon
micturition)
Carotid sinus
Passing out when shaving
hypersensitivity
(2015: when the patient
turns his heador wears a
tight collared shirt)
Hyperventilation
2015: Due to hypocapnia
syndrome
leading to loss of
consciousness
Hypoglycemia
2015: through intake of
oral hypoglycemics such
as glibenclamide,
metformin, insulin and
comistamil
Caveat:
Case 1
Diagnosis
Caveat

Doc, nahihilopo ako then loses consciousness

Trauma
Determine the differentials (this patient had trauma (head injury))
Temporal order is important (hitting head then getting up and fainting vs fainting and then falling and
hitting head)

II. IMPORTANCE OF HISTORY AND PE

Table 16. Importance of Hx and PE

Crombie, 1963
History and PE accounts for 88% of patient diagnosis
Hampton, 1975
History=82%
PE= 9%
Saundler, 1980
History=56%
PE= 15%
Sapira, 1990
History=90%
PE= 9%

Ian, Aca, Hannah

UPCM 2016A: XVI, Walang

Kapantay!

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OS 213: Cardiovascular System

LEC 02: CARDINAL SYMPTOMS OF HEART DISEASE
Exam 1 | Dr. Donato Maraon | September 24, 2012
Looking at the more recent values, we can see that we can still arrive at a diagnosis with history and PE. Between the
two, history is important!

Remember the importance of history taking (and PE) so we can prove this guy wrong: "Doctors pour drugs of
which they know little, to cure diseases of which they know less, into human beings of whom they know nothing".
Voltaire
END OF TRANSCRIPTION

Ian: Hi block A! One last module, then SEMBREAK na! Yehey! :)

Aca: Aca: Heaven in a wild flower. Also, Im currently in a post-Awkward (season 2) high. Matty please, please be the one! [cc: DOMS] They wont get to
read this, but happy happy birthday to my beloved batchmate, Blessie! I love you, sis Also to the sizzling hot and awesome Patrick (super miss na kita
) and lastly, belated happy birthday to one of the sausage masters, Lee! Kevin, awesome job, man. Sexy mo! Hi sisses and brods, AFTG! XVI: Walang
Kapantay! Hi you!
Hannah: Kamustamus Kalabasa naman sa minigreetings?! Hahaha! Sorry guys! We did our best but we guess our best was the best.
(vangagaboomboomangpakalakapeg!)

Ian, Aca, Hannah

UPCM 2016A: XVI, Walang

Kapantay!

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