Transcript Disorders of the Cardiovascular System

Clinical Cardiology
OVerview
By
Ragab abd elsalam ( MD)
Prof. of Cardiology
Approach to Patient with Heart Disease
1- Symptoms of Heart Disease = 2° myocardial ischemia
= disturbances of the contraction
system / and or relaxation of myocardium
= obstruction of blood flow
= disturbances of the contraction
= abnormal cardiac rate
2- Symptom Relationship to Etiology
- ischemia = manifest as chest pain
- disturbance contraction or relaxation = weakness /
fatigue Severe cyanosis, hypotension, syncope, increased
intra-vascular pressure
CHEST PAIN
Two categories:
Recurrent, often paroxysmal pain, which
is mild or moderate in intensity.
Prolonged & severe pain which is
commonly asscoiated with clinical
evidence of acute, serious illness.
(1) Recurrent chest pain:
(a) Angina pectoris:
Characteristics of anginal pain:
It is “visceral” pain: poorly localized and squeezing, oppressive,
burning or heavy in quality.
Duration: brief, usually it is lasting 2 to 10 min. & it is rarely
longer or shorter.
Usually it is mild or moderate in intensity.
Site: it is typicaly retrosternal, but it may occur in other locations.
Even then at least a portion of the pain is commonly beneath the
sternum.
The pain may be referred to precordium, neck, lower jaws,
shoulders, arms, back and epigasterium. Radiation to the left
shoulder and arm is especially common.
Precipitations: effort or emotional stress, after meals, exposure
to cold air or wind.
N.B.: Anginal pain may be excluded
under the following circumstances:
– If it can be localized with one finger.
– If it consistently last less than 30 sec. or longer
than 30 min.
– If it is sticking, jabbing or throbbing.
– If it occurs exclusively at rest with two
exceptions:
•
•
Pre-infarction angina.
Variant form of angina, described by prinzmetal,
vasospasm of coronaries usually is the leading cause.
– If the intensity of the pain is consistently severe.
Musculoskeletal chest pain:
Characteristics:
Radicular in nature.
The pain usually occurs at night.
It is usually precipitated by fatigue, incorrect posture and
movement of the involved segments but not movement of
the body as a whole.
It may be intensified with coughing or sneezing.
The discomfort is usually dull and aching, and may be
sharp.
The pain usually lasts for hours at time.
It is usually relieved by rest, analgesics postural exercises
and local heat.
Tioetze’s syndrome:
- Costochondral and chondrosternal pain, or swelling or
both.
- The pain is usually well localized, but may radiate
across the chest and over to the arms.
-Tenderness on palpation over the involved articulations.
Rib pain: may be due to trauma. Rib tumour causes
pain if it is metastatic in origin.
-Pain is usually described as sharp or burning and
reproduced by local pressure.
Fleeting, jabbing, lancinating or sticking pains are
common in many normal individuals.
The thoracic outlet syndromes
(e.g. the scalenus anterior, costoclavicular
hyperabduction cervical rib-syndrome), may cause
chest pain.
–
Symptoms depend on whether neural or vascular
structures are compressed at the thoracic outlet.
- Nerve compression is the common cause of pain
and paresthesia. It may be associated with a
demonstrable weakness.
- Vascular compression is quite rare, as venous
obstruction by thrombosis.
Shoulder disorders:
1. May cause pain that is referred to chest.
2. Careful analysis usually reveals that pain is
aggravated by shoulder movement, not the body
motion.
3. There is local tenderness and pain. Passive
movement and limitation of motion are commonly
present.
Less common causes: herpes zoster and Mondor
disease (superficial phlebitis of thoracic wall and
chest).
Psychogenic pain :
The discomfort of angina may be mimicked by anxiety
states.
It may take various forms :
–
–
–
Intermittent sharp, knifelike pains.
Persistent precordial aching unrelated to effort.
Tight sensations in chest.
It is commonly associated with sighing respiration and
symptoms owing to hyperventillation.
There is an important statement, that is mentioned by
the patient, “ the pain is coming from the heart”
DACOSTA'S SYNDROME:
- Psychogenic pain usually localized to
the cardiac apex. May be associated
with anxiety.
- It May be also associated
palpitations, hyperventilation, dyspnea,
weakness, depression, or other signs
of anxiety.
Pain due to pulmonary hypertension:
-The cause of pain may be:
-Right ventricular ischemia
- Enlarged right ventricle &
pulmonary artery may compress
on chest &sternum.
Pain associated with valvular diseases:
(a) mitral valve prolapse:
The pain may be due to :
tension on base of the redundant leaflet.
Tension on chordae tendinae and papillary
muscle.
Friction effect of redundant leaflet on
myocardium.
Associated with syndrome X.
Associated with gastrointestinal cause of pain.
Coincidental chest pain.
Aortic Regurgitation:
–The pain usually nocturnal. (Nocturnal
Angina).
–It is termed Angina of Lewis.
–May be related to baradycardia occurs
at night and marked decrease in the
diastolic pressure.
Prolonged chest pain
Prolonged, severe, protracted chest
pain may be the result of serious
underlying disease, such as
myocardial infarction, therefore,
immediate hospitalization of patients
for proper diagnosis and therapy is
mandatory.
(a) Acute myocardial infarction:
(b) Pain due to Aortic Dissection:
(c) Acute pericarditis:
Three types of pain may occur in acute pericarditis:
Pleuritic pain is the most common type.
Steady, severe retrosternal pain of sudden onset, simulating
pain of acute myocardial infarction.
The rarest type is pain at the cardiac apex felt
synchronously with each heart beat.
Characteristics:
– The pain is commonly sharp increased by breathing deeply,
swallowing and lying supine. It is sometimes relieved by sitting-up
and leaning forward.
– The pain is most commonly located in the precordial region and
may radiate to the neck or left shoulder
Mediastinal Emphysema:
Free air in the mediastinum produces chest
tightness and dyspnea.
** Hamman's Sign: Crunching, rasping
sound heard synchronous with the
heartbeat, indicative of mediastinal
emphysema.
Reminders
Angina pectoris: angina is a discomfort in chest or
adjacent area that is associated with myocardial ischemia
without necrosis. It is due to an imbalance in myocardial
oxygen supply and demand.
Stable (Typical) Angina: Angina upon effort, or angina
induced by increased blood pressure or increased heartrate. Angina is relieved by nitroglycerin, although
nitroglycerin is not specific to this type of angina.
* Levine's Sign: Patient makes fist and
holds it up to his chest, to describe the pain.
Second-wind Phenomenon: If
patient repeats same activity after the attack,
he may not feel the attack again the second
time.
Walk-through Angina: The pain subsides as
patient continues the activity.
Atypical Angina: Atypical presentation of typical angina.
Atypical Symptoms: Sharp or stabbing pain, rather than
crushing pain.
Atypical Causes: Angina with change in position, for
example, rather than angina strictly upon effort.
Angina Equivalents: Other symptoms that are caused
by myocardial ischemia.
> Exertional dyspnea.
> Nausea, indigestion.
> Dizziness, sweating.
Unstable Angina: Angina even at rest, or angina
that has recently gotten worse. It is associated with
sharply increased risk for myocardial infarct within 4
months.
Angina Decubitus is a specific term for angina
occurring at rest.
Variant Angina (Prinzmetal Angina):
Paradoxic angina occurring during rest but usually
not during exercise. It is caused by coronary
artery spasm. It can be hard to spot because it can
coexist with typical angina.
Clinical presentation of
patients with chest pain:
It can be divided into three
subsets:
Typical angina pectoris.
Atypical angina pectoris.
Non-anginal chest pain.
Dyspnea
Definitions :
It is the patient complaint of:
- shortness of breath.
or - he can’t get enough breath.
or - awareness of respiration.
It is subjective distress complaint of difficult breathing.
It is one of the most common distressing symptom in
cardiovascular disease.
Types:
- Dyspnea on effort (exertional
dyspnea).
- Orthopnea.
- Paroxysmal nocturnal dyspnea.
- Acute pulmonary edema.
- Cheyne-Stokes Breathing.
- Dry non-productive cough.
* According to the cause, dyspnea may
be:
Cardiac causes of dyspnea.
Non-cardiac causes of dyspnea.
Lung diseases.
Anxiety.
Anemia.
Thyrotoxicosis.
False-dyspneas in:
Pregnancy  “huff and puff”
Compansatory hyperpnea associated with metabolic
acidosis due to diabetes mellitus and uremia.
(a)Dyspnea on effort:
it is a common complaint. It is usually due to congestive heart
failure or chronic pulmonary disease.
* It is necessary to establish the degree of activity requiring to
produce dyspnea.
- What is about the daily activity of the patient?
- When the patient began to notice increasing dyspnea?
* When dyspnea is associated with wheezing:
If the patient is an adult especially over 40 years old, heart failure
is the foremost in the mind of the physician.
If there is a history of periodic wheezing and dyspnea since
childhood, bronchial asthma and lung disease is more likely to be
the cause of dyspnea.
It is important to remember that long standing pulmonary disease
may develop heart disease and heart failure. Also heart failure
may precipitate more bronchial asthma.
Orthopnea:
It implies that the patient has more dyspnea when he is
lying down.
The patient relates that he must use two or three
pillows in order to have a restful night.
Orthopnea is often associated with congestive heart
failure, but may also be associated with severe lung
disease. The fatigue associated with the exertion of
breathing seems to be less when dyspnea is due to
pulmonary disease than when it is due to heart failure.
Ask the patient:
1. Does the dyspnea occur whether the patient lies on
back, left or right side?.
2. Is it improved with digitalis & diuretic?.
3. Does it being within a half minute of lying flat?
4. Is the patient not completely free of dyspnea at any
chest elevation (severe mitral stenosis).
5. Is the dyspnea developed rapidly and for less than one
minute in supine position and then feels no dyspnea?
(suggest pulmonary hypertension).
(c) paroxysmal Nocturnal Dyspnea:
Characteristically, the patient goes to bed and has little
difficulty going to sleep in the recumbent position.
One or two hours later he is awakened from sleep with
acute shortness of breath.
He seeks relief by sitting upright, perhaps on the side of
the bed, or he even sits in a chair.
He occasionally goes to the open window searching for air.
After a time he becomes comfortable and returns to bed.
He may then sleep comfortably the remainder of the night.
 It is almost specific for left side heart failure.
 The only other causes for this unusual sequence of
events are:
- Hyperventillation syndrome due to anxiety.
Pulmonary emboli.
(1) For pulmonary emboli: it would be most unusual for
pulmonary emboli to occur for very many nights at the
same hour.
(2) For hyperventilation syndrome due to anxiety: It is
not so clearly relieved by sitting-up and is associated with
other signs suggesting this syndrome, such as tingling of
arms and hands and other evidence of anxiety.
ASK about:
1. How long after sleeping does it occur? (Redistribution of fluid
takes 2-4 hours to raise left atrial pressure).
2. Does the patient angle legs to get relief?.
3. Duration? (10-30 minutes).
4. Is it associated with cough, wheezing or frothy, pink sputum?
5. Obstructive sleep apnea? History of heavy snoring?
6. Paroxysmol nocturnal dyspnea usually occure in patients who are
suffering also from exertional dyspnea and orthopnea.
7. The precipitating factors of the attack is uncertain and probably
variable. Cough, bad dreams, slipping position, turning to side on
which he is ordinary dyspneic and abdominal distension are
among those suggested factors.
(d) Acute Pulmonary Edema:
The patient experiences the sudden development of
dyspnea and cough and he may produce frothy
blood-tinged sputum.
This symptom may occur without previous warning as in
myocardial infarction, or its may be preceded by
cardiac asthma or dyspnea on effort.
(e) Cheyne-Stokes breathing:
Periods of hyperpnea which alternate with periods of apnea.
This type of breathing occurs in:
1. Older patients with heart failure, hypertension or
cerebrovascular accident
2. It is associated with: Hypoventillation syndrome of obesity
(pickwickian syndrome)  the breathing is periodic in
nature, but it is not typical as chyne-stoke breathing.
3. Rarely occurs in children or in patients with core pulmonale.
(f) Dry non-productive cough:
1. Cough may on occasion the earliest symptom, the most
prominent symptom or the only apparent symptom of left
ventricular failure.
2. * Cough is an important symptom in certain forms of
cardiovascular diseases, even in absence of heart failure :
3. Aortic aneurysm with compression on bronchus or trachea.
4. Mitral stenosis with aneurysmally dilated left atrium.
5. Markedly dilated pulmonary artery.
6. Congenital double aortic arch forming a vascular
compression ring around the trachea.
Trepopnea:
Dyspnea that occurs in only one of several
recombent positions not due to congestive heart
failure:
(a) Cardiomegally.
(b) Musculoskeletal.
Platypnea:
It is the dyspnea provoked by sitting-up.
1. Left atrial myxoma.
2. Ball-valve thrombus of left atrium.
3. Orthostatic hypotension.
N.B.:
Some patient with angina pectoris, may complaint of
dyspnea rather than chest pain. This is termed (Angina
equavelent).
Clinical significance of orthopnea:
1. It is usually the result of heart disease (as many as 95% cases). It
reflects, a severe lung congestion on lying supine in patients with left
sided heart disease.
2. In about 5% of causes, are related to lung diseases:
3. Chronic obstructive lung disease (COLD) with apical bullae, where
the sitting position, not only improves the gas exchange but also, lung
mechanics.
N.B.:
1. patients with COLD, usually have a sitting-up and either clasping the
side of the bed or pushing over their thighs, producing the formation of
two patches of hyperpigmented callus immediately above the knees
(Dahl’s sign.).
2. Orthopnea in asthmatic patient is usually a sign of severity. If it is
observed at time of emergency, it is a good predictor of poor outcome.
Paroxysmal Nocturnal dyspnea (PND).
It is sought to be specific for Left sided heart disease and
failure, but:
Patient with chronic obstructive lung disease (COLD) may
have PND due to excessive secretion upon lying down.
Asthmatic patients also may have PND due to night
worsening bronchospasm.
Orthopnea:
Occurs in patients with heart failure, but also may occur in
patients with COLD due to partial loss of diaphragmatic
and accessory muscle function when supine.
Palpitation
It is a disagreable awarness of the
heart beat. The patient may use some
other terms and report as “pounding”,
‘stopping”, “jumping”, or “racing” in the
chest. The patient may complain when
the heart beat is slow, fast or irregular.
If there is a history of palpitations:
1.
2.
1.
2.
3.
4.
5.
6.
7.
8.
(a) Orientation:
When did they begin?
Ask about: shortest, and longest duration and the length of time
between attacks.
(b) Types and rate: ask about.
Regular or irregular.
Sustained or occasionally, strong beats.
Onset and offset.
 gradual  sinus tachycardia.
 sudden  ectopic tachycardia.
Rest or exercise.
Associated symptoms.
Maneuvers or medications that stop it.
Hemoptysis
Definition :
It means coughing-up blood.
Brisk bleeding: is commonly associated with specific focal
ulceration of the bronchus, such as” (bronchogenic carcinoma,
foreign body, or bronchiectasis).
Slow bleeding: Strongly suggest venous bleeding and is more
likely to be the result of increased pulmonary vascular resistance,
with secondary increase in flow through the bronchial venous
system such as may occur as a result of mitral stenosis or
bronchiectasis.
It is also helpful to notice whether the expectorated blood is
admixed with sputum or pus. This is valuable, as the site of origin
of the bleeding could be determined. Intimate admixture of blood
and pus are signs pointing to a deep-seated site of pulmonary
suppuration such as pyogenic lung abscess.
Three conditions must never be overlooked as causes of
hemoptysis:
(1) Mitral stenosis:
1. It is frequently induced by physical exercise, sexual intercourse,
or marked excitement.
2. It may be the first symptom, and may occur during pregnancy.
3. The blood comes from a break in the pulmonary veins, which
rupture under high pressure.
4. Apoplexy: occurs in 10% of cases with reversible pulmonary
hypertension due to rupture of broncho-pulmonary venous
varicosities. This type tend to subside as the vein adapt to high
pressure and as pulmonary arteriolar disease develops.
2) Pulmonary infarction:
Frank hemoptysis occurs in the minority of instances.
When hemoptysis occurs in a patient with heart
failure, pulmonary infarction is likely.
The bloody sputum usually appears from a few hours
to a day after the embolus.
(3) Eisenmenger physiology:
1.
2.
3.
4.
Patients with severe pulmonary hypertension
associated with atrial septal defect, or patent ductus
arteriosus, may have hemoptysis, secondary to
rupture of pulmonary capillaries.
Four additional rare causes of hemoptysis:
Rupture of a pulmonary arteriovenous fistula.
Rupture of aortic aneurysm into the trachea or
bronchus.
Pulmonary hemosiderosis.
Bronchial ulceration due to foreign body.
Cyanosis
Definition :
Bluish coloration of skin and mucous membrane.
Cyanosis cannot occur when the hemoglobin is less than
33 percent of normal since reduced hemoglobin cannot be
produced in an amount sufficient to cause the bluish color
(Five grams of reduced hemoglobin is needed for
cyanosis to occur). When the hemoglobin is normal, about
one-third of it must be in the reduced form for the bluish
color to appear.
* Clinical significance of history of
cyanosis:
If cyanosis is present only during the
neonatal period the possibility of an atrial
septal defect with temporarily reversed flow
(right-to-left shunt) during the neonatal
period is suggested.
– However, the most common causes of
neonatal cyanosis are, atelectasis, pneumonia,
or even occasionally from cerebral damage.
Persistent and severe neonatal cyanosis
suggests a right-to-left shunt often with
marked impairment of pulmonary blood
flow:
1.
2.
3.
4.
Tetralogy of Fallot with pulmonary atresia.
The hypoplastic left ventricular syndrome.
Tricuspid atresia.
Sometimes transposition of great vessels.
Cyanosis that develops after a few years of life
suggests a less severe form of tetralogy of
Fallot, in about of 75% or more. Cyanosis often
appeas following delayed closure of a patent
ductus arteriosus, or when child begins to walk.
Cyanosis occuring later in life of childhood
is suggestive of Eisenmenger complex (N.B.
Occasionally cyanosis may be present early in
life with this disorder, but not common).
Patients with trialogy of Fallot (atrial septal
defect and pulmonary stenosis), usually describe
history of cyanosis, late in (childhood or
A history of squatting with severe cyanosis (Hypoxic
spells), are most suggestive of:
–
–
Tetralogy of Fallot.
Trialogy of Fallot.
-
tricuspid atresia.
N.B.
–
–
Squatting seldom occur in Eisenmenger syndrome.
The squatting usually occur to relieve dyspnea and spells of
unconsciousness, with severe cyanosis.
In adults cyanosis and digital clubbing may be caused by
right-to-left- shunting. Such shunting is most often the result of
the Eisenmenger syndrome and occasionally of tetralogy or
trialogy of fallot or Ebstein’s anomally, or partial transposition of
the great vessels.
Adult cyanosis also may result from chronic or acute
pulmonary disease.
Adult cyanosis also may result from chronic or acute
pulmonary disease.
Chronic disease as:
Chronic obstructive lung disease.
Hypoventillation syndromes.
Pulmonary infiltrative diseases as Hamman-Rich
syndrome, sarcoidosis, metastatic cancer or severe
bronchiectasis.
Acute disease:
 Pneumonia.
 Pulmonary embolism.
 But the patient seldom complains of cyanosis in these
problems.
Cyanosis due to stagnant hypoxia:
Distal parts of extremities usually cyanosed in advanced
heart failure.
Cyanotic hands may be due to local stagnation called
(Acrocyanosis).
Rarely, cyanosis is caused by chronic or acute
methemoglobinemia, or apparent cyanosis by argyria,
which causes a bluish-gray discoloration of the nail beds
and mucosae associated with prolonged use of nose
drops containing silver.
Acute cyanosis in patients with chronic heart failure,
should suggest the possibility of associated pulmonary
embolism.
Very specific physiologic implication can
be made when differential cyanosis is
found:
(1) Cyanosis of the fingers greater than that of the toes
suggests complete transposition of great vessels with
either a preductal coarctation or complete interruption of
aortic arch and pulmonary hypertension with reversed
shunt through a patent ductus arteriosus delivering
oxygenated blood to the lower extremities.
N.B. If the left arm is slightly less cyanotic than right arm,
the coarctation of aorta is suggested. On the other hand if
both arms are intensely cyanosed, complete aortic
interruption is suggested.
(2) Cyanosis and clubbing of the toes associated with pink finger
nails of right hand and minimal cyanosis and clubbing of left hand
are suggestive of pulmonary hypertension with reversed shunt
through patent ductus arteriosus with normally related great
vessels.
(3) If the right hand is pink and the left hand and lower extremities are
intensely cyanosed, this suggest, that the right subclavian artery
arises proximal to aortic obstruction, plus patent ductus arteriosus
and pulmonary hypertension.
On the other hand, if the right subclavian artery originates
anomalously from the descending aorta, then both hands are
cyanotic.
Syncope
Definition:
It is a complete and transient loss of
consciousness due to inadequate cerebral
blood flow. The physician should bear in mind
that the commonest variety of syncope
(vasodepressor syncope) is not caused by
organic heart disease, or by organic disease
of the circulation.
Clinical significance:
Syncope that occurs in a threatening situation, such as
venipuncture suggests simple vasodepressor syncope.
A history of syncope since childhood when associated
with organic heart disease, may suggest the possibility
of congenital aortic stenosis.
Syncopal spells occur with tetralogy of Fallot, in such
a case, it is associated with dyspnea & cyanosis.
In children syncope rarely occurs in primary pulmonary
hypertension.
Syncope seldom occurs in congenital complete
atrioventricular (AV) block since the heart rate is usually
greater than 55/min. and the cardiac output reasonably
well maintained.
In older patients a history of syncope may be related to
one of several variaties of organic heart diseases:
If the patient is thought to have mitral stenosis, a history
of syncope may be very significant, it seldom occurs
with uncomplicated mitral stenosis. Such a history
suggests the possibility of a left atrial myxoma, or ballvalve thrombus with intermittent obstruction to left
ventricular filling.
Syncope in patient with ESM & LVH :
–
–
If typically occurs with exercise suggests aortic stelosis.
If it occurs after stopping exercise suggests HOCM.
A history of syncope in patient with angina should raise the
possibility of aortic valvular stenosis.
Syncope rarely occurs in patient with ischemic heart disease,
although occasionally it occurs at the outset of acute
myocardial infarction.
Syncope may occur in patients who have paroxysmal
tachycardia.
Syncope may be the initial symptom of massive pulmonary
embolism.
Syncope that occurs while shaving or while suddenly turning
the head, especially when wearing a tight collar, suggests
carotid sinus syncope.
It is important to have a history of the
position in which syncope occurs. The patient may
become light-headed or giddy when first arising in
the morning and becomes more able to tolerate
the upright posture during the day. This history
suggests orthostatic hypotension.
Syncope, which is associated with
memory defects, temporary hemiparesis,
paraplegia, vertigo or tinuitus in an older patient
suggests that vertebrobasilar artery insufficiency
may be responsible.
It is a heterogeneous symptom,
including sensations of vertigo,
presyncope, disequilibrium and lightheadedness.
It is one of the most complaint in
general medical clinics. It is often selflimiting and only rarely relates to lifethreatening events, even in elderly
patients.
*Common causes include:
Peripheral vestibular vertigo, labyrinthitis, Meniere’s
disease
Central vestibular cerbellovascular tumor.
Psychiatric disorders and hyperventilation usually in
younger patients.
Multicausal.
** Blurring of vision and even petit mal epilepsy may be
revered as dizzy spells
Giddiness:
blurring of vision associated with altered consciousness and swaying
sensation.
Vertigo:
Literally it means “sense of turning”  “rotation” either of the one’s
body or of the surroundings.
** The history is an easy pointer to vertigo:
Patient reports objects in his environment spun around
Or his body was turning.
Or his head was spinning.
Sometimes he may state that the floor or walls seemed to undulate or
sank or rose-up toward him or he was feeling of to and fro or up-and
down movement of the body, usually head.
The symptoms of vertigo are usually paroxysmal and of short duration
but may be chronic following acute attack.
It is accompanied by varying degrees of nausea and vomiting,
nystagmus headache and ataxia, as well as by the need to avoid
movement of the head.
Edema
Definition:
It is an increase in the volume of interstitial fluid
(i.e., the extravascular portion of the
extracellular compartment). The plasma
volume may or may not be increased.
** Interstitial fluid volume may increase
considerably before it is clinically appreciated.
** Edema is considered a symptom and a sign.
It is important to ascertain whether
edema of the extremities preceded
or followed dyspnea on effort.
Edema of cardiac origin is usually
preceded by dyspnea, and usually
associated with dyspnea except
with tricuspid stenosis.
Edema of one leg:
1. - Varicose veins.
2. - Thrombophlebitis.
3. - Lymphedema.
Periorbital edema:
1. It is common in children than adult.
2. It is common due to renal causes, but
may occur in heart failure.
3. ** Rare causes of periorbital edema:
(superior vena caval obstruction, and
trichinosis).
Ascitis:
It is recognized by the patient as an increase in girth or
swelling of the abdomen.
Ascitis due to heart failure is uncommon to day and
usually follows peripheral edema.
A local factor such as cirrhosis is also suggested when
ascitis associated with heart failure, seem to be out of
proportion to peripheral edema.
Constrictive pericarditis and endomyocardial fibrosis are
rare causes of cardiac causes of ascitis.
In children:
1. Hepatomegally and ascitis are the
first symptoms & sign of cardiac
edema than peripheral edema due to:
2. Portal circulation of children is less
complaint.
3. Systemic circulation in children is
more complaint.
Edema is a symptom and also
it is a sign.
1. On examination it can be elicited as follows:
2. Press on the skin over a bony area with 3 fingers spread
apart for 10-30 seconds.
3. Feel and look of at the valleys produced.
It is of two types.
1. Slow edema: the pitting remains for more than 60
seconds, and it is usually due to congestion.
2. Fast edema: the pitting remains less than 40 seconds,
and it is usually due to hypoalbuminemia.
Fatigue
Definition:
It is a sense of weakness, described by the patients
variously as exhuastion, tiredness, lack of interest,
low vitality or a feeling of being “all in”.
It is often accompanied by a subjective sensation of
weakness and a strong desire to rest and sleep.
When a patient with heart disease is water-logged
or when there is pulmonary congestion due to heart
disease, the patient is likely to complain of dyspnea.
Fatigue in a cardiac patient may be due
to:
1. Heart failure.
2. The complain of fatigue may occur just before, during
or following myocardial infarction.
3. Fatigue may be the main complaint of patient with
myocardial ischemia.
4. Cardiovascular drugs:
–
–
–
Diuretics.
B-Blockers.
Antihypertensives that cause postural hypotension.
Hoarseness of voice
1. It is usually unrelated to cardiovascular disease.
2. It may occur in patients with:
3. Aortic aneurysm that involves the recurrent
laryngeal nerve.
4. Mitral stenosis, occasionally may cause
hoarseness (Ortner’s syndrome).
5. Pericardial effusion, may be related to
myxoedema which may produce a coarse, lowpitched voice.
6. Sometimes in patients with larger ductus
arteriosus.
Intermittent claudication
Intermittent pain of the skeletal muscles due to temporary
ischemia that is usually (but not always) caused by
atherosclerosis of the artery or arteries that supply a
particular anatomic part of the body.
It is produced by effort and relieved by discontinuing the
effort.
It is never related to emotional stress.
The arterial obstruction is located proximal to the site of
claudication.
Leriche syndrome; Intermittent claudication of the
thighs and buttocks, is caused by obstructive disease of
the iliac arteries or the terminal aorta.
Intermittent claudication of the masseter muscles
suggests takayasu disease.
The “blue toe” syndrome is caused by
cholesterol emboli of the toes from proximal
atherosclerotic lesions of the arteries proximal to the feet.
Acute and persistent pain in the calf, thigh or other muscle
group suggests an embolus to the artery or acute
thrombosis of an obstructive lesion.
Cardiac cachexia
Mechanisms:
1. Poor eating and digestion: due to gastrointestinal
congestion and anorexia.
2. Poor absorption also due to gastrointestinal
congestion.
3. Deficit metabolism: liver congestion.
4. Tumor necrosis factors, play an important
role in initiation and prolonged cardiac cachexia .
 All of these factors lead to caloric, protein and
vitamin malnutrition.
Significance Of The
History As a pointer to
the Diagnosis
Cardiomyopathy
Hypertrophic cardiomyopathy:
1. Family history of sudden death
2. Younger or middle-aged patient.
3. Anginal pain or syncope, after but not during
exertion.
4. Recurrent attacks of palpitation.
5. Worsening of the symptoms on digitalis therapy.
Dilated cardiomyopathy:
– Influenza-like illness, followed by symptoms
& signs of heart failures.
– Short-term, history of dyspnea.
– History of drug-intake that is known to
cause myocardial depression.
– Peripartum symptoms & signs of HF
suggestive of Peripartum CM.
Restrictive Cardiomyopathy
1. History of frequent blood transfusion, skin color changes,
recurrent arthritis, impotence with diabetes mellitus may
suggest hemochromatosis.
2. Recurrent attacks of bronchial asthma in young patient
with history of embolic manifestations may suggest
esinophilic restrictive cardiomyopathy.
3. History of attacks of postural hypotension, with skin
bleeding and scratching may suggest amyloidosis.
4. Recurrent eye symptoms (uveitis), history of kidney
stone and renal problems and recurrent attacks of
syncope may suggest sarcoidosis.
Cardiopulmonary disease
Chronic obstructive lung Disease
(COLD)
1. Heavy smoking history.
2. History of seasonal asthmatic attacks.
3. History of repeated asthmatic attacks since
childhood, helped with bronchodilator.
4. The patient may give a history of easier breathing
on leaning forward.
5. Chronic cough and wheezing.
6. Occupational history e.g (coal-miner workers).
Pulmonary emboli with corepulmonale:
1.
2.
3.
4.
5.
History of long sitting after surgery.
Pregnancy & delivery.
Trauma.
Phlebitis and oral contraceptives.
History of deep venous thrombosis.
History suggestive of Rheumatic
fever :
Polyarthritis:
–
–
–
–
–
–
Fleeting or migrating arthritis.
Redness, hotness & swelling.
Associated with complete loss of mobility.
Self-limited.
Shows a dramatic response to Aspirin therapy.
No permanent deformity.
History of fever with murmur.
long-acting of penicillin taking history.
Family history.
History of murmur during school examination, insurance or
military service.
Cyanosis:
Time of appearance:
1. Since birth: (transposition, Fallot’s tetralogy.)
2. Childhood: (Eisenmenger’s syndrome or Ebstein’s
anomaly)
3. Adult with pulmonary hypertension may suggest
ASD.
4. During infancy associated with crying or feeding,
may suggest Fallot’s tetralogy.
Squatting: may suggest.
1. Fallot’s tetralogy.
2. Pulmonary atresia.
3. Eisenmenger syndrome.
Differential cyanosis: suggests ductus
with Eisenmenger syndrome.
Stroke in cyanotic patient, considers cerebral
abscess e.g. in Fallot’s tetralogy.
Cyanosis & hemoptysis may suggest
congenital arteriovenous fistula.
History suggestive of pericardial
diseases:
1.
2.
3.
4.
5.
6.
Medical history:
Uremia
Metastatic carcinoma, lymphoma, leukemia.
Connective tissue disorders as rheumatoid arthritis.
History of skin rash after direct sun exposure
(systemic lupus)
History of tuberculosis.
Recent viremia.
1.
2.
3.
4.
5.
6.
7.
Medicinal history:
Chest radiation (recurrent).
Chemotherapy.
Isoniazid, or minoxidil.
Patient symptoms:
Chest pain: increased on lying flat and relieved on
leaning forward.
Epigastric pain 1-3 days before chest pain.
Abdominal swelling before lower limb edema and just
before beginning of dyspnea or simultaneous with
dyspnea on exertion.
Position and Expose.
First position the patient at 45
degree angle.
Get comfortable with your
surroundings, make sure the patient
and area is well lit, and make sure
that the patient is comfortable.
General Inspection (must be
1.
2.
3.
4.
performed from the end of the patients bed)
(if the examiner are standing at the end of
the bed, ask them to move!) Look for:
Dyspnea.
Cachexia (referred to as cardiac cachexia).
Irritability.
Obesity&…...
Elfen facies:
It is characterized by
1. Short and upturned nose.
2. Widely spaced eyes.
3. Full checks.
4. Wid mouth with patulous lips.
Deep husky voice, and friendly
personality.
It is often associated with:
1. Hypercalcemia.
2. Supravalvular aortic stenosis.
3. Mental retardation.
Corvisart’s facies:
It is characterized by:
Puffy, purplish and cyanotic & swollen
eyelids.
Shiny eyes.
* It is observed in patients with:
-Aortic regurgitation.
-Heart failure.
DeMusset’s facies:
It is the bobbing motion of the head, synchronous with hear tbeat.
Significance:
1.
2.
3.
4.
5.
It is first characterized as a typical facies of patient with AR.
It is neither sensitive nor specific.
In fact it is usually observed in hyperkinetic states (large stroke
volume).
There is a variant of DeMusset’s sign, seen in severe tricuspid
regurgitation but the bobbing of the head, tend, to be more
lateral as a result of the regurgitant column of blood rising along
the superior vena cava.
It may be observed in patient with massive left pleural effusion.
Mitral facies:
It is the face of mitral stenosis. It is
characterized by pink and slightly
cyanoticcheeks.
When patients with mitral stenosis develop
right-sided heart failure and tricuspid
regurgitation as a result of long-standing
pulmonary hypertension, the overall skin color
becomes sallow and often overty icteric. This
appearance contrasts quite well with
persistently cyanotic cheeks.
Facies of lupus erythematosus:
It is characterized by:
A classic malar, butterfly-like-rash,
and often involving the bridge of the
nose.
Acromegally.
1. Excessive growth of facial
bones.
2. Broad forehead.
3. Protruding mandible.
Hypothyroidism:
1.
2.
3.
4.
5.
6.
Dull face with distorted thick skin.
Coarse features.
Dry hair.
Puffy eyelids.
Enlarged tongue.
Loss of outer 1/3 of eye brows.
Butterfly Rashs:
Systemic lupus erythematosus is
associated with libman-sacks
endocarditis.
Malar flash, without Rash: may
be seen in patients with severe
mitral stenosis.
Edematous lids, loss of outer brow hair
& sleepy appearance  hypothyroidism.
Oculomotor palsy may suggest 
association of complete heart block.
Ectopia lentis,. Iridodonesis 
Marfan’s syndrome or Homocystinurea.
Blue sclerae may be found in:
1. Mafran’s syndrome.
2. Ehler’s-Danlos syndrome.
3. Osteogenesis imperfectae: Usually associated with
AR & MR.
Arcus senilis in patients under 40
years  hyperlipidemia.
A coloboma (fissure) of iris and choroid is a major
sign of the “Cat eye” syndrome is associated with:
total anomallous pulmonary venous drainage.
Cataract:
1. Marfan’s syndrome.
2. Down’s syndrome.
3. Homocystinurea.
Bacterial endocarditis:
may lead to infected emboli.
1. May present with severe ophthalmitis.
2. Subconjunctival hemorrhage.
3. Petechiae.
Jaundice:
It is not often seen with cardiac problems.
It may be seen in:
1. High output states due to hepatic cirrhosis and alcoholic
hepatitis & may be associated with cardiomyopathy.
2. Cardiac cirrhosis due to advanced and long-standing
heart failure.
3. Pulmonary embolism and infarction.
4. Red-cell hemolysis due to prosthetic valves.
N.B.: The serum billirubin level seldom rises above 6
mg/100 ml, even in severe heart failure. If it is above 6
mg/100 ml, additional problem plus heart failure is
suspected.
Clubbing and cyanosis:
These are typical of congenital heart disease or pulmonary
arteriovenous fistula with a right to left shunt.
Differential cyanosis and clubbing:
It has a specific physiologic implication:
Cyanosis of fingers is greater than that of the toes;
suggests transposition of great vessels with either a
preductal coarctation or complete aortic arch interruption
with pulmonary hypertension, and reversed shunt.
In this case, if the left arm is less cyanotic than right,
coarctation of aorta is suggested.
On the other hand, if the cyanosis is intense and
symmetrically, aortic arch interruption is suggested.
Cyanosis and clubbing of the toes,
associated pink fingernails of right hand and
minimal cyanosis of left hand: this suggests
patent ductus arteriosus with normally
related vessels and pulmonary hypertension
with reversed shunt.
Cyanosis & clubbing of the toes and left
hand while the right hand is not cyonatic, this
suggests, the right subclavian artery arises
proximal to coarctation of aorta.
Reversed differential cyanosis:
Hands are cyanotic and clubbed, but the feet are
normal.
This occurs when there is right ventricular origin of
both great vessels, with concomitant disorder
including VSD, PDA & pulmonary hypertension 
oxygenated blood from LV enters the pulmonary
trunk through VSD, or from PDA into descending
aorta so the feet are normal. While the oxygendesatrurated blood from RV enters the ascending
aorta and brachiocephalic vessels so the upper
extremities are cyanosed and clubbed.
* Unilateral clubbing:
Aneurysm of aorta, or innominate/subclavian arteries.
Pancost’s tumour and lymphangitis.
Remember : DD of clubbing :
C = Cyanotic heart diseases
L = Lung diseases
U = Ulcerative colitis , Crohn,s diseases
B= Birth defect .
B=Biliary cirrhosis
I = Infective endocardits
N = Neoplasm ( es. Hodgkins)
G= Gastrointestinal malapsorption.
Red fingertips, “tuft erythema”: it may signify
small or intermittent right to left shunts with only
slight reduction in oxygen saturation.
Acute painful clubbing or hypertrophic
osteoarthropathy is a manifestation of bronchogenic
carcinoma, which may invade or metastasize to the
heart and pericardium.
Quinke’s pulsations: it is flushing of nail beds,
synchronously with heart beats. It is a sign of high
output states as aortic regurgitation.
Splinter hemorrhage; they are:
– Longitudinal, black and splinter shaped.
– Usually located in the distal third of the nail.
* Differential diagnosis: remember (SPLINT)
–
–
–
–
–
–
S= Sepsis
P= PAN /SLE/ RA
L=Limey ( Vit.C deficiency)
I = Infective endocarditis
N = Neoplasm
T = Trichomonas, trouma.
Osler’s nodes:
–
–
They are reddish purple, raised, tender nodules in the distal
pad of fingers or toes.
They suggest infective endocarditis
Janeway lesions : small non-tender raised
erythematous or hemorrhagic leasions of palms or soles:
–
They may suggest infective endocarditis.
Rheumatoid arthritis:
There is ulnar deviation of the fingers, thickening of the
middle interphalangeal joints, boxing of the wrists and
subcutaneous nodules.
Jacoud’s artheritis:
1. Marked ulner deviation at the metacarpophalangeal
joints.
2. It is almost always due to repeated attacks of rheumatic
fever activity.
3. * The deformity is due to periarticular fascial and tendon
fibrosis, rather than synovitis. So the fingers can be
moved freely into correct alignment.
Nail Color:
a) Leukonychia : White as in
hypoalbuminemia .
b) Wellow color : - Nicotine stains
- Wellow Nail Syndrome
( Peripheral edema , brochiactasis & pleural
effusion)
c) Blue nail: as in cyanosis , ochonosis , Bluered polycythemia .
d)Cherry red : CO poisoning.
e) Terry,s nails : the distal half is brow-red ,
while the proximal part is white-pink
occurs in - liver & in chronic renal failure .
f) Metanonychia : Multiple
brownishlongitudinal streaks.
Occurs in - Black person (normal)
- White person: melanoma
under fingernails
Obesity
Obesity may be central or peripheral. In fact its
location correlates strongly with its effect on health.
(a) Central obesity:
 Involves primarily the trunk and it is
characterized by:
A bihumeral diameter is greater than bitrochanteric
diameter.
Subcutaneous fat has a descending distribution and
is concentrated primerily in the upper half of the body
(neck, cheeks, shloulder, chest and upper abdomen).
b) Peripheral obesity:
Involves primerily the extremities, and it is characterized by:
A bitrochanteric diameter is greater than the bihumeral diameter.
Subcutaneous fat has an ascending distribution and is
concentrated primerily in the lower half of the body (lower
abdomen, pelvic girdle, buttocks, and thighs).
** Central obesity is more common in men, while
peripheral obesity is more common in women.
** Central obesity carries a much worse prognosis because of its
higher association with hypertension,diabetes, atherosclerotic
cardiovascular diseases, dyslipidemia and lower extremity venous
stasis diseases.
* Body Mass Index (BMI):
1. It is the federal government’s standard for body weight.
2. It is calculated as a ratio between weight and height and
provides a better measurement of body fat than the
traditional height and weight charts.
 According to old standards:
–
–
Men were considered overweight if they had BMI  27.3.
Women were considered overweight if they had BMI  27.8.
Revised guideline: Any one with BMI  25 is
considered abnormal
»Skin
signs
Amyloidosis:
1. Recurrent purpura; purpura in response
to minimal trauma to skin as gentle pinch.
This is due to fragile vascular wall, yellow
or reddish brown papules.
2. Amyloidosis may be primary or
secondary.
3. * Amyloidosis may be associated with:
2) Sarcoidosis:
- It is a granulomatous disease of unknown cause.
Sarcoid skin lesions:
1. Red, painful, tender nodules, of anterior portion
of lower extremity.
2. Sarcoid papules with atrophic centers, around
the nose and mouth.
3. May be diffuse with serpiginous borders.
4. In some cases, plaques may develop and
simulate psoriasis.
(3) Thyroid dysfunction:
(a) Hyperthyroidism:
1.
2.
3.
4.
Skin is warm and smooth.
Palms are pink and moist.
Nails may show oncholysis.
Pretibial myxoedema  flesh-colored plaques.
(b) Myxoedema:
1. Skin is puffy, dry and swollen but does not pit with pressure.
2. Slightly yellow color to the skin (as the carotene is
metabolized poorly by the liver).
3. Outer part of eyebrows may disappear and scalp hair may
become brittle.
4. Axillary and pubic hair become sparse.
Systemic lupus erythematosus:
(a) Skin is highly sensitive to sunlight:
1. Persistent flush & urticaria.
2. Descoid lesion scaly, reddish areas with follicular
plugging.
3. Ulcers may develop.
(b) Malar rash:
1. A reddish macular eruption, but may be urticarial.
2. Usually, found over, nose & cheeks  butterfly or bat wings
appearance.
3. (c) Telangiectasis, purpura, Raynaud’s phenomenon,
subcutaneous nodules and paniculitis may develop.
Scleroderma (Progressive
systemic sclerosis):
It is a connective tissue disease.
1. * Skin: It is tight, thick associated with vasculitis.
2. Raynaud’s phenomenon and ulcerations or scars of
finger digits.
3. Skin of the face may be affected  expressionless
& immobile skin around mouth.
4. Telangectasia and hyperpigmentation.
CREST syndrome:
1.
2.
3.
4.
5.
There are 4 out of 5 features are skin lesion:
Calcinosis  C.
Raynaud’s phenomenon  R
Esophageal dysfunction  E
Sclerodactyly  S
Telangiectasia  T
Diabetes mellitus:
1. Diabetic dermopathy: pigmented atrophic scars in the
pretibial areas.
2. Bullous diabeticorum: large bulous filled with blood, heald
without scars, in the hands, forearm, feet, & lower legs.
3. Eruptive xanthomas: small pinkish yellow papules with a
red base erupt on the buttocks and extensor surface of
forearms (Diabetes & hypertriglyceridemia).
4. Lipodystrophy: at the site of injection of insulin.
5. Necrobiosis lipoidica diabeticorum: Small red papules over
tibias  gradually increase in size  atrophic with red
border and yellow center.
6. Infant with diabetic mother  may develop hypertrophic
cardiomyopathy.
Hyperlipidemia:
1. -Xanthomatous lesions: localized
infiltration of lipid-containing
macrophages, that are located within the
tendons and skin.
2. Eruptive xanthomas.
3. Soft tuberous xanthomas.
4. Eye-lid xanthomas.
Hyperesinophilic syndrome:
1. Red hyperpigmented papules or
macules.
2. Uriticaria & angioedema.
3. Perifollicular papules.
4. Skin itches and scratch markers.
Endocarditis:
1. Skin lesions such as infected wounds or furuncles that
serve as a source for bacteremia and subsequent
endocarditis.
2. Skin lesion secondary to endocarditis:
3. Petechial hemorrhage of skin and mucous membrane.
4. Osler’s nodes.
5. Janeway lesions.
6. Splinter hemorrhage.
7. Finger clubbing.
Hemochromatosis: may be primary
(genetic) or secondary:
Excessive iron that deposits in tissues can cause
cirrhosis, diabetes mellitus, artheritis, hypogonadism
and cardiomyopathy.
Skin:
1. May has a bronze color due to hypermelanosis.
2. May be a salte-gray color due to hemosiderin.
3. The skin may become dry and scaly.
4. The hair may become sparse and spooning of nails may
occur.
Malignant Melanoma:
It is a cutaneous mole that changes in color, size, shape,
or consistency, or mole that itches or become painful.
Cardiovascular lesions:
1.
2.
3.
4.
5.
6.
Cardiac metastasis.
Charcoal heart.
Pericarditis & effusion  tamponade.
Arrhythmias.
- Conduction defects.
- Heart failure may occur.
Rheumatic fever:
1. Subcutaneous nodules: non-tender, non-movable
nodules occur on elbows, the forehead and bony
prominences.
2. Erythema marginatum: is a pin-black, with clear center,
and occurs on abdomen, trunk and proximal parts of
legs & arms.
* N.B.: Other causes of subcutaneous nodules &
erythema marginatum.
1. Rheumatoid arteritis.
2. Lupus erythematosus.
3. Annular erythema may occur in glumerulonephritis, drug
toxicity & sepsis.
Rheumatoid arthritis:
Early: transient rash of pink macules & papules on
the face, palms & soles in association with, low gradfever, months or years before artheritis.
Late: in adults there are rheumatoid nodules, these
are firm, movable subcutaneous nodules, (one to
several centimeters in size) & are painless. They are
found on the bony prominances.
Palmar erythema, purpura ulceration of skin due to
arteritis.
Raynaud’s phenomenon may occur.
ER.MARGINATUM
(i) Enlarged liver due to engorgement with
venous
blood that is not able to return to the failed
right heart
and (ii) impaired intestinal absorption due to
congested
intestinal veins secondary to congested liver
-Look for morphological features of
Marfan s Syndrome,
Down s Syndrome, Turner s Syndrome
(each of
which has cardiovascular sequelae).
-Look for any pacemaker, holter
monitor, or telimetry leads in situ. Also
look for GTN patches, Nicotine
patches, etc.
-Now peruse the bedside and look for
iv fluids, GTN spray or GTN patch, O2
prongs, TEDS, ECG pads, etc.
(3) Examination of the Hands.
Ask the patient to put both of his hands, palms
down, onto a pillow
Proceed to get down on your knees (a position you
will grow accustomed to as a medical student) and
inspect the hands of the patient, you may ask the
patient to lift the hands off the pillow to better view
the fingers especially, but it is important not to
touch the hands at this stage.
Once you proceed to touch the patients hands,
make sure to inquire first if there is any
pain in the hands.
Clubbing - look for the following stages
(which occur in this order)
(i) increased fluctuance (2 ways to
assess this
(a) place one thumb at the root of the nail
just at the end of the skin before the
cuticles arise, and place the other thumb
at the very end of the nail and see-saw the
pressure between the two thumbs or
(b) place one thumb on the
lateral most portion of the nail, and the other
thumb on the opposite lateral portion of the
nail and see-saw the pressure between
the thumbs.
Increased fluctuance feels boggy.
(ii) Loss of angle - this can be assessed using
Shamroths sign.
* This is performed by placing the patients
two index fingers together so that the nails are
face to face, and the most distal index
interphalangeal joints are touching (like forming
the M shape with your two index fingers).
* In this position, normal patient s have a
diamond shaped space between the two nails,
however in patient s
with second stage clubbing, there will be no space in
this position and thus loss
of angle can be pronounced.
(iii) Increased AP diameter - this is a
qualitative assessment, compare with your finger AP
diameter
(iv) Drumstick appearance of the pulps of your
fingers
(v) Hypertrophic Pulmonary
Osteoarthropathy
NOTE: make sure to look at the toes as well for
clubbing.
-Cyanosis (peripheral) which is due to
vasospasm
-Splinter Haemorrhages - which are
visible on the nail bed.
-If these are distal, they are most likely due to
manual labour.
-If they are proximal, they are likely to indicate a
vasulitic process.
-If they are proximal and tend to be linear and
parallel to the long axis of the nail this may well
be vasculitis due to infective endocarditis
Now look for Tendon Xanthomata (not
xanthelasma which occurs around the eye). This
is a yellow or orange deposition
of lipid in tendons which occurs in Type II
Hyperlipidemia
XANTHELASMA
(increased LDL).
This causes deposition over
tendons in the arms, hands and legs/feet
.-At this stage, kindly ask the patient to turn their
hands over
so that you may observe the palmar aspect of the hands
.-Osler s nodes - (O is for Osler as O is for Ouch)
– these are painful red raised nodules on the pads of the
fingers and/or toes which occur due to vasculitis
.-Janeway lesions -these are non-tender
erythematous maculopapular lesions which contain
bacteria and occur on the palmar aspect of the hands
and feet
Palmar xanthomata may occur but they
indicate a different abnormality to tendinous
xanthomata.
Palmar xanthomata and Tuberoeruptive xanthomata
(yellow/orange maculopapular rash which occur over
the elbow and/
or knee joints) both indicate Type III Hyperlipidemia
(increase in VLDL)
-Look for palmar crease pallour which may signify
anaemia.
* Examination of the Face:
Eyes:
Corneal arcus - donot call it arcus
sinilis, it implies the patient is senile and it is
a dated term. This is a yellow
ring around the iris which occurs in patients
with hypercholesterolemia. However, if it it
occurs in the elderly > 65yrs old, then it is
insignificant.
Sclerae - look for icterus (yellowing) which
may occur
with (1) severe congestion of the liver in heart failure
and (2) prosthetic valve induced haemolysis due to
excess turbulence.
Also look for blue sclerae which occurs in Marfan, s
Syndrome and Ehlers Danlos Syndrome and has
implications in terms of aneurysms and
dissections.
Facial Tissue
* Mitral Fascies - rosy cheeck with bluish
tinge of dilatation of malar capillaries
due to pulmonary hypertension secondary to
mitral stenosis)
* This can be distinguished from the Malar
Butterfly rash that occurs
in Systemic Lupus Erythematosus because in
SLE the rash doesnot spare the
bridge of the nose, in mitral fascies it does.
Mouth:
Shine a pen torch onto the roof of the
patients mouth.
A high arched palate signifies Marfan s
syndrome (genetically predisposed to
Aortic root dilatations, Mitral Valve
Prolapse,
Aortic Dissections and Aneurysms.)
Enlarged tongue:
1. Amyloidosis.
2. Glycogen storage disease.
3. Hurler’s syndrome.
4. Down’s syndrome.
5. Hypothyroidism.
Orange, large lobulated tonsils
 occurs in Tangier disease (type of
hyperlipidemia.)
Petechiae on buccal mucosa,
occurs in bacterial endocarditis.
A high arched palate can be
observed in Marfan’s syndrome.
Cleft palate is associated with
1.
2.
3.
4.
a high incidence of different types
of congenital heart disease:
Atrial septal defect.
Patent ductus arteriosus .
Dextrocardia.
Coarctation of aorta.
* Xanthelasma which are yellow
lipid deposits around the eyes
and which occur in type II or type III
hyperlipidemia.
* Look for blood vessels on the iris of
the patient (called Rubeosis)and it
occurs in poorly controlled
diabetic patients.
Look for cataracts which
occur in poorly controlled diabetic
patients (it occurs due to high levels
of blood glucose being converted
to sorbitol by aldose reductase in
the eye which deposits as cataracts
Look for Hypertensive changes:
(1) Silver Wiring due to hardening of retina
(2) arteries
(2) Arterio Venous (AV) Nicking or Nipping
(where the hardened
arteries indent the softer veins).
(3)Exudates
(4)Papilloedema - enlarged optic nerve
insertion due to
increased pressure CSF pressure which
occurs with hypertension
(Papilloedema is required to be present
for malignant hypertension
to be pronounced)
** Taking of the Pulse
It is important to turn the patientshand palm side up
for taking the pulse, or else the exainer will not be
able to view what it is you are doing.
@Assess the Rate: Normal is 60 - 100 beats per
minute.
Bradycardia is < 60 and Tachycardia is >100.
Assess the Rhythm:
(i) Regular (consistent predictable
beat),
(ii) Irregularly irregular (inconsistent
unpredictable beat which occurs in atrial fibrillation),
and (iii) Regularly irregular (inconsistent but
predictable pattern to the beat – which occurs in
Second Degree Mobitz Type I (Wenckebach)
Heart Block which is increasingly prolonged PR
intervals (on ECG) followed by a dropped QRS at
which point the PR shortens and then lengthens
progressively again until QRS is dropped again, and
so on)
or Sinus arrhythmia
which is increased pulse on
inspiration due to increased
venous return, and
decreased pulse on
expiration (it is normal).
@Assess the character of the
pulse: Note that the character of
the pulse is poorly assessed by the radial pulse.
Rather, the carotid or brachial pulse should be
used to assess the brachial pulse.
Water Hammer Pulse: this is checked by
raising the
patients arms while assessing the pulse.
The pulse bolus can be felt to fall back towards
the patient and this is significant of Aortic
Regurgitation (you are in effect creating a
hydrostatic pressure increase into the valve by
raising the arm and so the pulse which is a
blood ejection bolus impinges on the
incompetent valve)
(ii) Slow Rising Plateau Pulse: This is a
pulse that has a slow rising bolus under your finger,
but then the bolus itself lasts for a long time before it
slowly comes down.
It can be likened to feeling a long worm sliding
past your finger as you feel the pulse.
This signifies aortic stenosis.
(iii) Pulsus Alterans: This is a pulse that is
strong
one minute,then weak the next. This signifies Left
Ventricular Failure.
@Assess the volume of the pulse:
> The volume is increased in aortic
regurgitation, and decreased in aortic stenosis.
It can be best described as the loudness of the pulse
under your finger.
> And it is a qualitative measure of the pulse pressure.
Since in aortic regurgitation the diastolic pressure is so low
(as blood slips back into the left ventricle from the
aorta), then the ejection of the over-filled ventricular
blood in systole will cause a dramatic increase
in pressure.
>This will feel like a loud pulse under the examiners fingers.
@Assess Radio-Radial Delay:
Feel for the radial pulses in both arms
simultaneously. If any delay is detected,
this may signify
a large arterial occlusion by large
atherosclerotic plaque or aneurysmal
process
Look at the Tongue and Lips for central
cyanosis (defined as > or equal to 5mg/dl
of deoxyhemoglobin in the blood.
This is interesting because it is more difficult for
patients with anaemia to reach this concentration
of deoxyhemoglobin and so more difficult for them
to become centrally cyanosed,
even though they may have greater difficulty
oxygenating their blood)
Look at the mucosa (inner part of the lips) for
petechiae (which isvasculitic and may signify
infective endocarditis)
Look at the tongue and note any
enlargement which may occur due to amyloidosis
(amyloidosis can cause restrictive
cardiomyopathy).
(7) Examination of the Neck:
Carotid Arteries
Inspect the neck area for carotid
endarterectomy scars
Palpate the carotid arteries.
NEVER palpate both carotids simultaneously,
you may occlude the
majority of the cerebral perfusion and thus
cause your patient to faint
....and a big fat fail to ensue as your exam mark.
Palpate for the character of the pulse which
can be as follows:
Also, on palpating the carotid
artery, it is important to evaluate the
-
presence of systolic thrill, that may be
produced by:
Carotid atherosclerosis.
Kinking of carotid arteries.
Valvular aortic stenosis.
Carotid shudders in severe aortic
regurgitation.
* Anacrotic - means small volume, slow
uptake, notched wave on upstroke indicative of
aortic stenosis.
* Plateau - means a prolonged but
diminished upstroke, is also indicative of aortic
stenosis.
* Biferiens - is the term used for anacrotic and
collapsing pulse which occurs when the patient has
both aortic stenosis and regurgitation
simultaneously.
* Alterans - strong and weak beats
interchanging irregularly - indicative of
Left Ventricular Failure
* Jerky pulse - strong and spike of a
pulse wave - indicative of Hypertrophic
Cardiomyopathy.
Abnormalities of Arterial Pulse:
I. General Abnormalities:
The size of the arterial pulse is determined by:
- Left ventricular stroke volume.
- Rate of ejection.
- Distensibility of the systemic arterial bed.
- Peripheral resistance.
- Systolic and diastolic pressures.
- The distance between the heart and the palpated
artery.
*There are two clinical abnormalities of
the pulse size:
a) Hypokinetic  Small, weak pulse.
b) Hyperkinetic large, strong pulse.
So on palpation of an artery, one should
obtain an impression of both the height of
pulse pressure and the rate of pressure
pulse change.
Hypokinetic Pulse
Weak and small pulse
Occurs in conditions with:
1. Low stroke volume of left ventricle
2. A narrow pulse pressure.
3. Increased peripheral vascular
resistance.
Common causes:
–Left ventricular failure.
–Constrictive pericarditis and
tamponade.
–Valvular stenosis (aortic, mitral,
tricuspid or pulmonary)
- Shock, tachycardia...).
Hyperkinetic Pulse
The pulse pressure shows a rapid rates of
rise.
It may be
a) Rapid rates of rise with normal
size:
This is termed: (Jerky or Brisky Pulse).
Occurs in:
Double way of left ventricular ejection, as in:
– Mitral regurgitation.
– Ventricular septal defect (VSD).
Hypertrophic obstructive cardiomyopathy
(HOCM): where there is no obstruction until the
outflow tract contracts and approximates the
thickened septum to mitral valve. The hypertrophied
muscles of LV ejects about 80% of blood before
obstruction.
b) Pulse of rapid rate rise with increased pulse
pressure.
1- Bounding pulse: rapid rates of rise with increased pulse
pressure, but with normal contour.
2- Collapsing or water hummer pulse, sometimes termed
Corrigan’s pulse: Exaggeration of bounding pulse, where
there is a short and sharp peak, with contour change, as
the wave is transmitted peripherally.
The rapid upstroke and downstroke tend to be exaggerated
as the pulse wave is transmitted peripherally. So these
abnormalities are often better appreciated by palpating
the brachial and radial arteries than palpating carotid
arteries
Hyperkinetic pulse is usually
associated with:
1.
2.
3.
4.
Increased stroke volume of left ventricle
Wide pulse pressure.
Decrease in peripheral resistance.
Hyperkinetic circulatory states, may be
considered in three main categories:
1- Hyperkinetic states with
NORMAL hearts:
1. Fever.
2. Pregnant females secondary to
arteriovenous shunt in the
placenta
3. Hyperthyrodism, anemia..., etc
2- Hyperkinetic states due to abnormally
rapid run-off of blood from arterial system:
-Shunting of blood from aorta: (patent
ductus arteriosus, aortopulmonary septal
defect, rupture of a sinus of valsalva into
the right atrium or right ventricle).
- Large peripheral arterio-venous fistula:
(Congenital, traumatic, mycotic  etc).
- Small multiple arterio-venous fistula: (Pajet’s
disease of bone, cirrhosis of the liver).
- Aortic regurgitation  moderate to severe.
- Occasionally severe mitral regurgitation.
3) Complete Heart Block with bradycardia,
 increased strok volume.
(II) Specific abnormalities:
A) Pulsus Parvus et Tardus:
It describes a small pulse with a delayed systolic
peak.
- This pulse has a delayed peak, so it is termed
(plateau) pulse.
- When the aortic stenosis is severe the anacrotic
notch is easily observed in the ascending limb, so it
is also termed (anacrotic) pulse.
- This type of pulse is characteristic of aortic
stenosis of at least moderate severity.
N.B.
Systolic thrill is usually palpated over carotids &
usually occurs between anacrotic notch and the
peak.
The character of this pulse may be disappeared in
patients with left ventricular failure, and in patients
with concomitent mitral stenosis.
Some elderly patients with calcific aortic stenosis may
have nearly normal carotid pulse inspite of severe
obstruction due to rigid aorta, as a result of
atherosclerotic changes, so the aorta is unable to
expand.
In supravalvular aortic stenosis, also
the patient has a plateau pulse, but
can be differentiated by:
Difference in pulse volume between both arms.
Right sided carotid thrill.
Blood pressure is higher in the right arm than the
left.
Characteristic facies (Elfen Face).
B) Double Beat = Twice -beating pulse:
This term is applied when two waves are
palpated during each cardiac cycle. The
second wave may be palpated either
during systole or diastole.
Dicrotic Pulse.
The Second wave is palpated during diastole.
It is produced by accentuation and palpable
dicrotic wave following the second heart sound.
Palpated in both carotid and peripheral arteries.
The dicrotic wave becomes
palpable when there are:
Low cardiac output.
Soft and elastic aorta.
High peripheral resistance
The most common causes of palpable
dicrotic wave are:
Severe congestive heart failure as in (DCM).
Tamponade.
The low output state following open heart surgery, especially
aortic valve replacement.
Fever.(typhoid fever)
Anacrotic Pulse:
Exaggeration of anacrotic notch gives palpable two wave
during systole as in aortic stenosis (Severe).
Pulsus Bisferiens: Bis = twice &
feriens = beating:
Causes and Mechanisms
HOCM:
> Upstroke or ascending limb  rises
initially very rapidly and forcefully. (an
initial systolic wave  (Percussion
Wave).
> Systolic dip:  due to sudden decrease
in the rate of left ventricular ejection, as the
obstruction becomes significant.
> Tidal wave:  Follows the systolic dip,
and produced by continued but slower
decelerated ventricular ejection, and
reflected wave from periphery.
> The percussion wave is usually higher than
the tidal wave.
Significance :
It is characteristic of Hypertrophic obstructive
cardiomyopathy and it may be the first clinical clue
of HOCM.
It may be possible to bring out the characteristic
bisferiens pulse by performing valsalva maneuver
or by exercise.
In combined Aortic stenosis (AS) and Aortic
regurgitation (AR)
The aortic regurgitation should be at least of
moderate severity.
The bisferiens pulse may be palpated in pure
Aortic Regurgitation which should be severe.
Also bernouli effect is the underlying
mechanism.
** There is an important feature that can
differentiate the bisferiens pulse in HOCM
from other causes of pulsus bisfierience;
which is the character of pulse following
extrasystoles:
- In HOCM, the pulse is very small
following extrasystoles, where more
contraction causes more obstruction.
- In other causes, in normal the
pulse wave is strong after extrasystole
(post-extrasystolic potentiation)
=(pulse is exaggerated than normal).
Pulsus Alternans
There is a regular alternation of the height of the pressure
pulses, but the beats occur at a regular intervals.
Frequently, may be more readily detected while taking the
arm blood pressure.
There is alternation of left ventricular contractile force.
Alternation of LV end-diastolic volume and stroke volume.
Sometimes alternation of LV end-diastolic pressure
** mechanisms
Sudden critical change in diastolic filling period.
Alternation in the number of cardiac fibres contributing to each
systole.
Significance:
- May be associated with third heart sound (S3)
- May be observed after premature ventricular
contraction or tachycardia in heart failure without
pulsus alternans.
- Latent pulsus alternans: in some patient with heart
failure, without apparent pulsus alternans, the
characteristic pulse can be exaggerated by:
> Upright position.
> Nitroglycerine therapy.
> Exercise.
D) Pulsus Bigeminus :
It is the most common cause of peripheral arterial
pulsations that alternate in size from beat to
beat:
The strong pulsation occurs after long diastolic
filling phase following the premature beat.
The weak pulse occurs due to weak premature
beat.
Significance:
It is commonly associated with digitalis toxicity.
E) Pulsus paradoxus:
Normally the systolic blood pressure
usually declines (5-10 mm.Hg) during
inspiration.
** Best observed by careful
measurement of blood pressure.
** It is due to relative pooling of
blood in the pulmonary vasculature during
inspiration, as a result of lung expansion
and of the more negative intrathoracic
pressure. In addition transmission of the
negative intrathoracic pressure to aorta and
great vessels.
** So pulsus paradoxus is exaggeration of the
normal: the declines in the systolic pressure
during inspiration is more than 10 mm.Hg.
Significance:
* Pulsus paradoxus may be produced by conditions
which:
- Limit the inspiratory increase in blood flow to right
ventricle and pulmonary artery.
- Cause a greater than normal amount of inspiratory
pooling of blood in the lungs.
- Cause the intrathoracic pressure to have very wide
extremes of pressure during inspiration and expiration.
- Interfere with venous return to either atrium relatively
more during inspiration, e.g abnormal inspiratory
increase in pericardial pressure.
** Several clinical conditions are associated
with pulsus paradoxus:
> Superior vena cava obstruction.
> Asthma, emphysema and airway obstruction.
> Pulmonary embolism.
> Severe heart failure
> Cardiac tamponade due to pericardial effusion.
> Constrictive pericarditis.
> May occur in patients with severe hypotension 
shock.
N.B: Patients with cardiac tamponade
have pulsus paradoxus.
- Also may have kussmaul’s sign (a truly
paradoxic finding), which is an increase in
peripheral venous distension during
inspiration.
-
Mechanism: change in the pericardial
shape  rises the intrapericardial pressure
 obstructs venous return to the heart.
In contrast to this the pulsus paradoxus
that occurs with pulmonary diseases
(asthma, emphysema... etc) have marked
exaggeration of the normal expiratory
increase in venous pressure.
*So this is of great diagnostic importance
that differentiate pulsus paradoxus in patient
with pericardial diseases from that in patients
with pulmonary disease
Blood Pressure Measurement:
=First make sure that the blood pressure cuff you are
utilising is the right size for the patient (this is done
by placing the width of the cuff around the arm
, for it to be accurate, the width of the cuff needs to be
approximately of the circumference of the arm.
This is significant because a cuff that is too large for
the patient over estimates blood pressure and a cuff
that is too small for the patient under
estimates the blood pressure.
=Sit the patient down or keep them lying in the bed but sit
them up at 45 degree angle.
* Too-narrow and too-large cuff:
* A too-narrow cuff may give false higher
reading in systolic pressure up-to 50 mmHg, due
to higher inflation pressure is needed to inflate
the cuff.
* A too- large cuff may give false low blood
pressure.
* On begining deflation of cuff the release
should be slowly to avoid spasm of artery at the
begining.
=First find the systolic pressure by inflating the
cuff while feeling for the radial pulse. (Do not use the
stethoscope yet). The pressure at which the pulse
first disappears is the systolic pressure. This is done
first because it allows you to estimated what range
you; d expect the systolic pressure to be in this
patientbefore commencing auscultation.
..
=Deflate the cuff.
Now position the stethoscope over the brachial
artery, and inflate the cuff again until the
pulse sounds are no longer heard.
..Now deflate the cuff at about
3-4mmHg per second until
the first pulsation is heard again
(this is the first Karatkoff sound).
..Continue to deflate the cuff until
absolutely no more sounds
are heard anymore (the very last
turbulent sound will
be that of the 5th Karatkoff sound).
=Repeat the process in the other arm.
Note that the BP can
vary between arms by up to 10mmHg and still
be normal.
=Now Repeat the Blood Pressure in the patient
while theyare standing. If systolic blood pressure
falls by >15mmHg or diastolic pressure falls
>10mmHg then one can pronouncethe patient
has postural hypotension (the gold standard test is
the Tilt Table Test where the BP and ECG is
taken at 3 minute intervals while the patient is
Tilted in a special table from the horizontal position
To the vertical in increments of 15 degrees
* Auscultatory gap:
> It is the silence caused by the disappearance of
korotkoff sounds after the first appearance of the true
systolic pressure, and reappearance of pressure
(some 10-20 mm.Hg lower ).
> It requires venous distension of the forearm and
concomitant low flow.
-To avoid it:
Determine the systolic blood pressure first by palpitory
method.
Routinely ask the patient to clench his first 10 times and
inflate the cuff rapidly.
* Pseudo-hypertension:
> Misleadingly high systolic, diastolic or mean
blood pressure measured by cuff compared with
the pressure measured directly by intra arterial
needle.
> Observed in medial necrosis of brachial artery
(Monckeberg arteriosclerosis).
--- Pipesteam calcified brachial artery.
* Pseudohypertension is
suspected in elderly:
> Disproportionate elevation of blood pressure to
clinical findings: (no ECG. evidence of LVH, no
cardiomegaly in X-ray).
> A palpable radial pulse after the brachial pulse
has been eliminated by inflation of the cuff above
systolic pressure. (Osler’s sign
maneuver)
• Subclavian Steal:
> the use of a vertebral artery as a collateral
circulation to feed the subclavian artery (usually
on the left).
> Blood from a vertebral artery flows
retrogradely into the distal subclavian, thus
“stealing” blood from the brain causes vertibrobasilar insufficiency and the blood pressure is
lower in one arm than other.
Pulse pressure:
It is the difference between systolic and diastolic
blood pressure: ( thus in patient with systolic
blood pressure of 120 mmHg, and diastolic
blood pressure of 80 mmHg, the pulse pressure
is 40 mmHg ).
-Abnormally
narrowed pulse
pressure:
The pulse is considered abnormally narrowed if it is
less than 25% of the systolic value. (For example, a
patient with systolic blood pressure of 100 mmHg
and diastolic pressure of 90 mmHg has a pulse
pressure of 10 mmHg (
Causes:
a- The most common cause is a drop in left
ventricular stroke volume, as in patients with
obstruction to left ventricular filling or left ventricular
emptying (e.g.: tamponade, constrictive pericarditis
or aortic stenosis.(
b- It may be observed in extreme tachycardia, in
which the filling time of ventricle is reduced.
c- It may be seen in shock as a result of increased
peripheral resistance.
-* Reversed pulsus paradoxus:
> It is an increase in systolic blood pressure that
coincides with inspiration rather than expiration.
> It is observed in :
1- Hypertrophic cardiomyopthy: it is a typical sign due to
(stiff septum) & reversed inspiratory movement.
2- Some cases of severe left ventricular failure (stiff &
less compliant ventricle).
3- Positive-pressure ventilation reverses the respiratory
changes in intra- thoracic pressure.
Neck Vein
The bedside examination of the pulsations in the
neck veins is the clinical key to the dynamics
of the right side of the heart.
Two main objectives should be observed:
> Study of the wave form of pulsations.
> Venous pressure.
* Principles of studying the Neck
Veins:
1- It is necessary to examine both internal and external
jugular veins on both sides as well as venous pulsations
which may be visible in the suprasternal notch or in the
supraclavicular fossa.
2-The right IJV is superior for accurate evaluation of venous
wave form due to:
- Direct continuouty with RA.
- Innominate vein may be compressed by the arch of
the aorta, making the left sided venous pressure to
be abnormally high in normals.
* Position of the patient:
> The trunk of the body should be elevated until
maximum pulsation is noted.
> In most normal subjects the maximum pulsation is
usually observed when the trunk is inclined less than
45 (15-30) degree.
Sit the patient up at 45 degree angle
with their head turned away from you
Remember you are always on the
patient,s right side,
So you will be viewing the right JVP.
Although both can be viewed,
the right JVP is actually closer to the
right atrium and so functions
as a more accurate manometer of
right atrial pressures).
Look for a pulsation between the
two heads of the
sternocleidomastoid
muscle (the clavicular insertions). This
is the site of the internal jugular
vein, and it is the internal jugular vein
that is used for JVP because
the external jugular vein is too
tortuous for good measurement and
viewing.
•Light should be tangential to illuminate
•highlights and shadows.
•Neck should not be sharply flexed.
•Using a centimeter ruler, measure the
•vertical distance between the angle of Louis
•(manubrio sternal joint) and the highest
•level of jugular vein pulsation.
• A straight edge intersecting the ruler
• at a right angle may be helpful.
You will assess the JVP for Height
and Character:
Height - the height is measured from the
sternal angle (of Louis) in a line
perpidicular to the floor.
* JVP is considered raised if > 3cm
(note: some may say it is raised if >8cm
and the reason for this is that some people
are purists, and so they consider the right
atrium as 0cm.
Now since the angle of louis is 5 cm
above the right atrium,one simply adds 5
cm to any measurement above the angle of
Louis for this method of JVP
measurement,so donot let that throw you).
A raised JVP indicates a raised
Right Atrial Pressure which can
be from many conditions ie Fluid Overload
(iatrogenic), Right Ventricular Fialure.
* Character of the JVP - The
wave form of the JVP is complex and
you will not be expected to comment on
subtle changes in
these wave forms in different
patients.
* But you will be expected
to know the normal wave form
and some pathological manifestations.
Technique A: Jugular Venous
Pressure Measurement (JVP)
**NB:
1-The neck muscles especially sternomastoid should
be relaxed because if it is tense it will obscure
pulsations so place small pillow under the neck or
gentle massage by your hand.
2-The head should not rotated or if necessary for few
degrees only to avoid tense of neck muscles.
3-Proper evaluation of venous pulsations is possible
only when they are correlated with all events of the
cardiac cycle.
4- Carotid pulse may be used to time venous pulse.
Heart sounds are preferable for timing.
Jugular Vein
Carotid Artery
No pulsations palpable.
Palpable pulsations.
Pulsations obliterated by pressure
above the clavicle.
Pulsations not obliterated by
pressure above the clavicle.
Level of pulse wave decreased on
inspiration; increased on
expiration.
No effects of respiration on pulse.
Usually two pulsations per systole
(x and y descents).
One pulsation per systole.
Prominent descents.
Descents not prominent.
Pulsations sometimes more
prominent with abnominal
pressure.
No effect of abdominal pressure on
pulsations.
The normal wave form is composed of
the following in order:
A wave, C wave, X - descent, V wave,
Y-descent.
A wave – Atrial contraction, C wave Closure of tricuspid, X - descent ,
relaXation of atrium, V wave - atrial filling
(Filling), and
Y-descent - emptYing of atrium.
* (a-wave):
Mechanism:
> Retrograde transmission of the pressure pulse
produced by atrial contraction, where there is a
brief backward flow of blood from right atrium to
venae cavae.
>It is the prominent positive wave in normal.
> It is a presystolic wave begins just before first
HS.
> Occurs at the moment of (S4) if present
* (C-wave):
It is a brief positive wave that interruptes the
descent of venous pulse from the summit of (awave).
Mechanism:
> Impact of carotid artery adjacent to vein so it is
termed (carotid impact)
> Retrograde transmission of pressure pulse due
to bulging of TV into RA during RV systole.
* (V-wave):
Mechanism:
> During ventricular systole the TV is closed, but
blood continues to fill the venae cavae and RA
leading to increase in the volume and pressure
within them. So the pressure rises from the
trough of (x-wave) to the positive (v-wave).
> The 2nd HS occurs shortly prior to the summit of
v-wave which marks the opening of TV.
* (X-wave) = Systolic Collapse:
Occurs in late systole, shortly before the 2nd HS.
Mechanism:
> Downward displacement of the base of the
ventricles including TV during ventricular Systole
 fall in RA pressure.
> Continued atrial Relaxation.
* (Y- wave) = Diastolic collapse:
Mechanism:
V-wave descent caused by opening of TV & rapid
rush of blood from RA to RV.
Ascending limb of Y-wave is produced by
continued diastolic inflow of blood into the great
veins, RA & RV (which are in free
communication during diastole).
The S3 of right side occurs at the moment of Y
trough while the S3 of left side occurs shortly
before the trough.
Manometer of right atrial
pressure.
Function at waveform
ASK ME:
points:
• Atrial filling
• Systole
• Klosed tricuspid
• Maximal atrial filling
• Emptying of atrium
Abnormalities of The Venous Pulse:
Abnormalities of (a-wave):
a-wave is normally the dominant wave and tends
to increase during inspiration inspite of the
decrease in venous pressure.
Abnormalities involves: their timing & amplitude.
Timing:
Absent a-wave  in atrial fibrillation due to absent
atrial contraction.
• Venous pulsation in AF:
Absent a-wave.
Decreased or obliterated X-descent or even systolic expansion.
The predominant wave is Y-descent.
Irregularity of the pulsations.
• In sinus tachycardia
a-wave may
be fused with the preceding v-wave & so be
diminutive or even absent.
• * When a discrete a-wave with
ascending and descending limbs is clearly seen
to be completed prior to the first HS it occurs in
prolonged P-R. (First Degree HB).
Amplitude:
1- Prominent a-wave: Observed when the
right atrium contracts against decreased
compliance of RV as in pulmonary hypertension
& acute pulmonary Embolism.
2- Giant a-wave: Observed when RA
contracts against obstruction:
- Tricuspid stenosis, Tricuspid atresia
- Severe pulmonary stenosis
3-Cannon-wave:
Occurs when the RA contracts against closed TV during
RV systole  So the resulting wave is the fusion of
(a,c & v) waves.
* Significance
> Regular connon waves:
AV-junctional Rhythm.
> Irregular Cannon –waves:
Most common type & it is of great diagnostic importance
observed in:
Ventricular premature beats.
Complete HB  in this type the wave may be longer than
arterial pulse.
Ventricular tachycardia.
Abnormalities of the systolic
collapse (x-wave):
In tricuspid regurgitation this collapse may
be:
 Decreased or
 Obliterated
 or even replaced by a positive wave.
This depends on the degree of tricuspid
regurgitation (TR):
> Mild TR decreases the systolic collapse.
> Moderate TR causes obliteration or small
regurgitant (r-wave).
> severe TR  systolic expansion  large r-wave.
** in this case  S wave or what is called
Arterialization of neck vein, or, ventricularization of
neck vein.
** In constrictive pericarditis :
The predominant wave is sharp deep Ydescent.
X-descent is shallow.
N.B : X-descent may be prominent & deep than Ydescent if it is associated with active pericaiditis.
Abnormalities of the
diastolic collapse (Ywave).
The down slope of the Y descent or V-wave
depends on:
Height of RA & great venous pressure
Pressure -volume relation between RA & great veins
Rate of venous return.
Resistance to forward flow across TV.
Ventricular compliance.
RV. impedance.
Slow & shallow Y descent  tricuspid
stenosis.
 Sharp, deep & rapid Y-descent is observed
in Constrictive Pericarditis
Patients with severe HF.
* They are differentiated by the Lancisi’s Sign
Lancisi’s Sign : large regurgitant systolic wave
(systolic expansion)  characteristic of severe TR
in HF, not in constrictive pericarditis.
Jugular Venous Pulse (JVP):
The JVP has the following
characteristics remembered by :
MOPHAIR >>
M - Multiple Wave Form,
O - Occludable,
P - Positionally dependent ,
H - Hepatojugular reflux is present,
A - Above (fills from Above),
I - Impalpable,
R - Respiratory changes ).
IV- Venous Pressure:
> Normally the internal Jugular vein is collapsed except
in its lower part.
> The degree of congestion of the neck veins reflects
the pressure in the right atrium.
> The venous pressure is said to be elevated when the
venous column in the neck is more than 4 cm above
the zero reference point.
** The angle of lewis is the zero reference.
*** Clinically the medial end of the clavicle in 45°
inclined position is the best clinical reference
where the angle of lewis and medial end of the
clavicle at the same level. so examination on 45°
is the best.
** The level of the clavicle in sitting position is
above the angle of lewis whereas in 45°
position, the sternal Angle is at the same level of
clavicle.
Estimation of central venous
pressure:
>First position the patient to get a good view of
the internal jugular and its oscillations.
> Identify the highest point of pulsation, which
usually occurs during exhalation and coincides
with the peak of the a and v waves.
> Find the sternal angle of lewis ( junction of the
manubrum with the body of the sternum).
> Measure the vertical distance from the
sternal angle to the top of the jugular
pulsations in centimeters. This distance
represents the jugular venous pressure
(JVP).
>This method relies on the that fact that the
center of the right atruim (in which venous
pressure is by convention zero) is
approximately 5 cm below the sternalangle of
lewis.
> This relationship occurs in peoples of normal
size, shape, regardless of body position.
> Thus, using the sternal angle as the reference
point (the vertical distance in centimeters to the
top of the column of the blood in the Jugular
vein) provides an adequate measurement of
JVP.
** JVP in turn is 5 cm lower than central
venous pressur (CVP). Thus CVP=JVP+5.
** Causes of congested
Neck veins.
- Right ventricular failure > The
most important cause .
- Raised intracardiac pressure:
- Constrictive pericarditis
- Pericardial effusion.
- Resistance to flow as in tricuspid
stenosis, tricuspid Atresia,
pulmonary hypertension.
- SVC obstruction: Congested
non-pulsating neck veins.
- Thrombus.
- Bronchogenic carcinoma.
- Retrosternal hugely enlarged
thyroid gland.
Dominant v wave [easily heard].
• Tricuspid regurgitation
Absent x descent
• Atrial fibrillation
Exaggerated x descent
• Cardiac tamponade
• Constrictive pericarditis
Sharp y descent
• Constrictive pericarditis
• Tricuspid regurgitation
Slow y descent
• Right atrial myxoma
Causes of elevated JVP
- Bradycardia
- Fluid overload [esp. IV infusion]
- RVF
- Constrictive pericarditis
- Pericardial effusion
- SVC obstruction
- Tricuspid stenosis or regurgitation
- Hyperdynamic circulation
- Raised Intra-thoracic pressure:
> Pleural Effusion
> Emphysema.
> Increased Blood volume:
> Acute nephritis.
> Large IV infusion.
> Pregnancy.
- High output states as in:
> Anaemia.
> Fever.
> Thyrotoxicosis.
> Arterio-vnous fistula.
> Beri-beri....etc.
*Hepatojugular (Abdominojugular
Reflux):
it is termed the one-minute
Abdominal compression tests: firm
pressure over the right upper quadrant of
the abdomen for 60 seconds.  Abnormal
elevation of the internal jugular pressure
indicates that the right ventricle cannot
accept the increased venous return caused
by abdominal compression.
**Kussmaul’s sign:  Paradoxic increase
in jugular venous distension during inspiration.
Observed in:
> Severe right – sided heart failure.
> Constrictive pericarditis.
> Right ventricular infarction.
> Restrictive cardiomyopathy.
> Tricuspid stenosis.
> Superior vena cava syndrome.
The external Jugulars are less
suited for venous pulsations
examination due to:
> They often become compressed while going
through the various fascial planes of neck.
> They have valves that may prevent adequate
transmission of right atrial pulsation.
> They are so constricted, in patients with
increased sympathetic activity.
> They are not in straight line with right atrium.
Jugular venous findings of a right
ventricular Infarction:
> The mean JVP is increased.
> Prominent a-wave.
> Prominent X and Y descents.
> Positive abdominojugular reflux.
> Concomitant tricuspid regurgitation, gives
additional findings (such as giant V-waves and
right earlobe bobbing ) .
Significance of neck veins in
differentiating the type of pericardial
disease:
* In tamponade: there is an X-descent but little or
no Y descent, where there is much restriction
from the begining of diastole.
* Constrictive pericarditis: there is a shallow Xdescent and deep Y descent, when the
restriction occurs only after the opening of
tricuspid valve.
* Effusive -constrictive pericarditis: the Xdescent is more or less equal to the Y- descent.
* Bernheim Effect:
left ventricle bulge into RV during diastole
prevents good RV filling, but does not
prevent the RV outflow (SO it is a type of
inflow obstruction, not an outflow
obstruction).
-Prominant a-wave.
-Decrease in Y-descent.
-Increase in X-descent.
** Occurs in:
> Chronic mitral regurgitation with dilated
left ventricle.
> Chronic LV hypertrophy:
> Aortic stenosis.
> Hypertrophic cardiomyopathy.
> Severe hypertension.
* Reversed Bernhiem:
in severe acute RV dilation,
interventricular septal bulge toward
the LV in diastole and reduce the LV
stroke volume causes:
> Palsus paradeoxicus.
> Lung congestion if it is severe causes
dyspnea.
* Sustained apex:
> It is the apex that remains outward throughout systole
and begins to fall a way only with second beart sound.
*Significance:
a- A significant finding of aortic stenosis.
b- May be due to ventricular aneurysm involving apex.
c- If the apex is palpated in axilla and it is sustained it may
be due to complete absence of pericardium.
d- In HOCM sustained apex means severe left ventricular
hypertrophy or in absence of LVH, it means decrease
in ejection fraction.
Palpable presystolic impulse at the apex:
> Atrial hump due to strong left atrial contraction & it
rounded in contour, it is usually felt in systolic
dysfunction.
 Palpable 4th heart sound: the palpable atrial
hump is termed palpable 4th heart sound. It is
sharp and associated with auscultated 4th heart
sounds.
 It is observed in patients with impaired diastolic
function and with normal systolic function as in
HOCM & in hypertension.
* Presystolic impulse is commonly
observed in HOCM, more than aortic
stenosis... How?
 In HOCM, although the interventricular septem is
very thick, where the strong atrial kick can easly
expand the rest of LV, which is not hypertrophied as
the septum.
 In AS: The entire LV is equally hypertrophied and
therefor resists expansion of left atrial contraction.
*Tracheal Tug:
(to diagnose aortic aneurysm of aortic
arch):
Stand behind the seated patient.
Apply steady upward pressure on the
cricoid cartilage by one finger  you
will readily detect the downward pull
on trachea with each aortic pulsation.
* Left parasternal pulsations:
a) A slight precordial lift may occur in children
normally.
b) Bulging of the precordium in children denotes
longstanding right ventricular enlargement.
c) A localized, sustained heaving lift in the lower
left parasternal region denotes right ventricular
hypertrophy due to pressure overload. (PS.)
d) A hyperdynamic impulse denotes right
ventricular volume overload as in (ASD) .
e) A left parasternal lift due to enlarged left
atrium.
* Continuous thrill:
> Infraclavicular patent ductus arteriosus.
> Root of neck  venous hum.
> Back:
- localized: arterio-venous fistula
- Posterior intercostal, spaces & apex of
scapulae  enlarged collaterals of
coarctation.
* Thrill on carotids:
- Bilateral systolic thrill (AS).
- Bilateral vibrations (carotid shudders).
- Unilateral:
- Right side;
> Supravalvular AS.
> Right sided kinking & atherosclerosis of
carotids.
- Left side;
> Pulmonary stenosis (transmitted).
> Left sided arteriosclerosis.
* Pulsations of the right
sternoclavicular Joints and right
sternum.
a) Pulsation of right joint may indicate rightsided aortic arch.
b) Aortic dissection or aneurysm.
c) Aneurysmally dilated RA & RV.
d)Dextrocardia.
* Auscultate the Carotid arteries for
any bruits.
It is important to know physically why a
bruit is
produced in any artery.
* There is an equation from physics
which describes the
parameters necessary to produce a bruit.
* In effect a bruit is the sound made
from turbulent flow.
The following is the equation which you
should commit to memory if you want high
honours:
(1) Either the flow is laminar or
(2) The carotid is completely 100% stenosed
thus producing no flow whatsoever.
This can be confirmed
because in a completely stenosed carotid artery,
the carotid pulse cannot be felt.
Abnormal waveform causes
* Dominant a wave
• Pulmonary stenosis
• Pulmonary hypertension
• Tricuspid stenosis
* Cannon a wave
• Complete heart block
• Paroxysmal nodal tachycardia
• Ventricular tachycardia
(8) EXAMINATION OF THE
PRECORDIUM:
Inspection:
-Look for scars: midline sternotomy is
CABG or valve repair,
left or right sided lateral thoracotomy
scars (check under female pendulous breasts)
which may indicat previous closed mitral
or tricuspid valvotomy.
-Look for abnormal rib cage: (i) Pectus
excavatum
(ii) Pectus carnatum (iii) Kyphoscoliosis.
* These can be caused by Marfan,s
syndrome
which may result in distortion of
the position
of the great vessel and
displacement of the apex beat.
* If severe, it can cause Pulmonary
Hypertension (secondary to a
reductionin pulmonary function).
-Look for pacemaker (under the
right or left pectoral muscle)
-Look for a visible apex beat
-Look for a visible pulmonary
artery pulsation due to severe
pulmonary hypertension.
* Palpation:
> Apex beat: always begin your palpation
of the apex beat from the axillae towards the
midline.
> Once you can palpate it (the size of a
2 euro coin) count dow the number of
spaces with the left hand while
maintaining position of the apex with
the right hand.
> Comment on the (i) Position of the
apex beat and (ii) Character of the Apex beat
(i)Position - the normal position of the
apex beat is 5th intercostal space on the
left, and 1 cm medial to
midclavicular line.
> If the apex beat is lateral or
inferior to this, it can indicate cardiac
enlargement, chest wall deformity, or
pleural/pulmonary disease.
(ii)Character - is described by the
following:
* Left vent. Thrust =Normal apex.
* Pressure Loaded - a sustained beat pressing
against your hand indicative of aortic stenosis or
hypertension.
* Volume Loaded - increased area of the palpated
beat which is indicative of left ventricular failure
(LVF).
** Therefore, the size of the apex beat is larger
than the normal 2 euro size.
.
Double Impulse (or triple)
- indicative of HOCM,
this occurs because the atria contract into
hardened ventricles causing a loud S4
sound that is palpable.
This loud S4 is palpable just before the
tapping of the ventricle that is the apex
beat thus giving rise to a double impulse
Tapping Apex - A palpable S1 (mitral or
tricuspid stenosis)
with a normal apex beat which follows.
The S1 is palpable in these stenoses
because the atria arestill trying to squeeze
blood passed the stenosed valve when the
ventricle contracts thus slamming the valve
shut (if you are trying to close a door while
someone on the other side is pushing it open,
when you finally close it....its gonna slam
shut.....same idea here).
Absent Apex - can be a finding if the
chest wall of the patient
is thick, if they have emphysema,
pericardial effusion, shock
(or death), or Dextrocardia from Kertagener,s
syndrome.
Parasternal Heave - felt left of
sternum
(interdigitate your
fingers in the intercostal spaces
and feel for any heaves)
this is indicative of Right
Ventricular Enlargement or
Severe Left Atrial Enlargement
Feel for a palpable P2 which is
indicative of Pulmonary
Hypertension
Feel for any thrills over the
relevant valve areas (if felt,see if it
corresponds with apex beat, if it
does it is a systolic thrill, if not then
it is diastolic)
Auscultation:
Hunt for a Murmur
-(always listen for HS I and II while listening
in all the areas)
-First place the bell of your stethoscope over
the mitral area
-Remember to apply the bell of your
stethoscope to the chest wall very lightly or else
a diaphragm is created by the stretched skin and
this defeats the purpose of using the bell
-The low pitched sounds that you would expect
to hear over this area are that of mitral stenosis
or the 3rd heart sound.
-Second place the diaphragm of your
stethoscope over the mitral area (to listen for
high frequency sounds).
-Thirdly place the diaphragm at the tricuspid
area (5th intercostal space, left sternal edge)
and auscultate any murmurs.
-Next place the diaphragm at the pulmonary area
(2nd intercostal space, left sternal edge) and auscultate
any murmurs.
-Next place the diaphragm at the aortic area
(2nd intercostal space, right sternal edge) and
auscultate any murmurs.
-Next ask the patient to sit forward and place the
diaphragm of your stethoscope between
both shoulder blades,
-Whenever you hear a murmur, make sure
to simultaneously
listen to the murmur and feel for a radial or
carotid pulse todetermine if the murmur is
systolic
(occurs with each beat of your pulse)
or diastolic (occurs in between each beat of
your pulse).
* Heart Sounds I,II, III, IV and the Split:
The following is the sort of abnormalities you
may hear when listening to the heart sounds:
Heart Sound I (which is the closure of the tricuspid
and mitral valves)
Loud HS I = occurs whenever the flow from the
atria to the ventricles is still high pressure and high
volume when the ventricles start contracting thus
closing these valves despite the continued
high pressure and high volume flow).
Soft HS I = occurs whenever the
pressured volume of flow from atria to
ventricles is long gone (the flow is
complete) , yet the ventricle has not
started contracting yet.
As a result, the closure of the valve
simply closes softly, donot coapt
* Loud A2 = if there is systemic
hypertension or aortic stenosis
* Loud P2 = in pulmonary hypertension
* Soft A2 or P2 = Aortic (pulmonary)
regurgitation or calcification
* Splitting:
** If you think you hear a split
second heart sound , note that normally the
aortic valve closes before the pulmonary
valve due to greater diastolic pressure
pushing back on the aortic valve.
Logically then, since inspiration causes
increased
venous return to the right side of the heart which
causes larger amount and stronger ejection of
venous blood pressing open the pulmonary valve
to gain access to the pulmonary artery, thus the
closing of the
PV is delayed further on inspiration
in relation to the closure of the AV.
** As a result, splitting of the two heart sounds
(I & II) is increased on inspiration.
First heart sound (S1)
1.Louder than
normal
2.Variable in
intensity
3.Diminished in
intensity
1.Mitral stenosis, short PR interval
2.Atrial fibrillation, complete heart
block
3.Mitral regurgitation, severe aortic
regurgitation, long PR interval,
calcified mitral valve
Second heart sound (S2)
1.Fixed splitting
2.Wide, physiologic
splitting
3.Paradoxical splitting
4.Increased intensity of A2
5.Increased intensity of P2
6.Decreased intensity of A2
7.Decreased intensity of P2
1.Atrial septal defect
2.Right bundle branch block,
pulmonic stenosis
3.Left bundle branch block,
aortic stenosis
4.Severe hypertension
5.Pulmonary hypertension
6.Calcific aortic stenosis
7.Pulmonic stenosis
Increased Splitting:occurs in pulmonary
stenosis, Right bundle branch block, and
Ventricular septal defects (because l
pressure is greater than R. pressure, the
right side becomes fluid overloaded).
Fixed Splitting:occurs in Atrial Septal
Defects and this occurs because of
equalisation of the 2 atrial pressures and
volumes and thus inability for change in
volume to occur on inspiration.
Paradoxical Splitting:occurs in aortic
stenosis, aortic coarctation, hypert. and a
large Patent ductus arteriosus which
increases the flow to the left
atria/ventricles and thus keeps aortic V
open longer thus delaying the A2
component of the second heart sound).
When one hears a splitting of the second heart
sound, it is impossible for you to ascertain whether
the split is a regular split (A2 followed by P2) or a
paradoxical split
(P2 followed by A2). The only way you can tell is
by auscultating while asking the patient to inspire.
If the splitting is increased, then it is a normal
split.
If the splitting is decreased, then it is a
paradoxical split (note that a paradoxical split
occurs when there is aortic stenosis).
Extra Heart Sounds:
NOTE: the extra heart sounds can only be heard if the
atria are contracting appropriately, as a result don t say
that you can hear the S3 sound right after saying that the
patient has Atrial Fibrillation, because this is impossible.
Remember this is the order or pattern of the heart
sounds
(note the relative distance between the sounds):
4th---------1st----------------------------------------2nd--------3rd
S3: a low pitched sound arises from the l or
R ventricles. It represents rapid ventricular
filling
(ie AR or mitral regurgitation) This sound can
be normal in young patient <40 yrs old and in
pregnant patients.
It occursbecause the ventricle is already
filled with fluid to the brim, so an extra
push of fluid
from the atrium causes the ventricle
to balloonout causing a low pitched
3rd HS. When it is present, the
rhythm that is heard is Ken----------Tu cky.
The Ken representing HS1, Turepresenting HS2, and ckyrepresenting HS3.
S4: a high pitched sound arises from the L or R
ventricles.
This sound occurs due to the atria contracting
fluid into a non-compliant ventricle.
This heart sound is always pathological if heard
and it may be due to anything which hardens the
ventricle be it hypertrophy or fibrosis (ie aortic
stenosis, hypertension, mitral regurgitation,
ischaemic heart disease (this heart sound may
present during angina or MI).
If HS3 and HS4 are present at the same
time, the sound is referred to a quadruple
gallop and it is representative of severe
ventricular dysfunction.
If the patient becomes tachycardic (HR >
100bts/min) while having HS3 and HS4
simultaneously, these two sounds can
become superimposed which is referred to
as a summation gallop.
Extra heart sounds
1.Third heart
sound (S3)
2.Fourth heart
sound (S4)
3.Opening snap
4.Ejection
sound
1.Markedly diminished left
ventricular diastolic function
2.Modestly diminished left
ventricular diastolic function
3.Mitral stenosis
4.Bicuspid aortic valve,
pulmonary valve stenosis
Additional Sounds:
Opening snap- occurs in mitral
stenosis or tricuspid stenosisand it
occurs because of difficult
of these valves in first opening.
Ejection Systolic Click - occurs in
aortic or pulmonary stenosis (due
specifically to bicuspid congenital
valves)
Non-Ejection Sytolic Click - occurs if there
are redundant mitral valve leaflets or an ASD
Tumour Plop (diastolic) - occurs when one
has an atrial myxoma (which occurs in the
atria thus the name) and so on diastole,
when the mitral or tricuspid valves open, the
tumour plops down into the tricuspid or
mitral valve opening.
Pericardial knock (diastolic) is a sudden cessation of ventricular filling
b/c of inability of the ventricle to expand
any further due to some restrictive
extrinsic boundary.
Thus, it tends to occur in constrictive
pericarditis.
Prosthetic Heart Valves - you should have
some idea of the differencesbetween ball-cage
valves and disc valves (both prosthetic),
xenograft tissue valves
(porcine valves) do not have a differentsound to
them because they are tissue!
Pacemaker Sound - is a late diastolic high
pitched click due to the contraction of the chest
wall muscle on pacemaker firing just before
ventricular contraction.
* Systolic murmurs:
The very vast majority of murmurs are systolic
When soft they are usually early in systole and
disturb the end of S1. S1 often appears slurred
in these cases as opposed to ending abruptly as
is normally the case
* Mid-late systolic murmurs.
The careful clinician focuses on the end of S1 for
soft systolic murmurs.
Holosystolic murmur: refers to a systolic
murmur
that begins during or immediately after S1 and ends
with the onset of S2
Pansystolic murmur: refers to a systolic
murmur that begins during or immediately after
S1 and continues into and obscures S2 (note that
left ventricular pressure ) continues to be greater
than left atrial pressure after aortic valve closure
– during isovolumetric contraction).
Systolic murmurs
1- Early
systolic
2Midsy
stolic
1-Acute, severe mitral regurgitation, low-pressure
tricuspid regurgitation
2-Aortic sclerosis, aortic dilatation, aortic stenosis,
pulmonic stenosis, hypertrophic cardiomyopathy,
increased aortic valve flow (can also be caused by
anemia, fever, or thyrotoxicosis)
3Holos 3-Mitral regurgitation, high-pressure tricuspid
ystolic regurgitation, ventricular septal defect
4-Late 4-Mitral valve prolapse
systolic
Diastolic murmurs:
- Less commen than systolic murmurs
- Low frequency
-Rather low intensity and so are graded
out of 4, not 6
-Best identified with the bell of the
stethoscope
-My be early diastolic , mid0diastolic
or late ( presystolic) murmurs.
Diastolic murmurs
1.
1-Early
diastolic
2.
2-Middiastolic
3.
3-Late
diastolic
1.Aortic regurgitation, high-pressure
pulmonary regurgitation
2.Mitral stenosis, tricuspid stenosis,
severe mitral regurgitation
3.Mitral stenosis, severe aortic
regurgitation (Austin Flint murmur),
left atrial myxoma
Continuous murmurs:
-Common
-Typically associated with a PDA, but also arteriovenous
fistulas
-Usually vary in intensity throughout the cardiac cycle,
however the murmur is detected at all times
-The continuous nature of the murmur may only be
noted at the PMI, while at other locations
it may only be systolic, for example.
To and Fro murmurs:
The name for the situation when a systolic murmur
and a diastolic murmur (due to different physiologic
etiologies) coexist.
Continuous murmurs
1.Peaks before and after S2
2.Rough, noisy, or high-pitched,
louder during diastole
3.Louder during systole
1.Patent ductus arteriosus
2.Normal venous hum
3.Mammary souffle
Intensity:
The intensity of the murmur at its origin is
related to (Blood flow velocity) x (Rate of
flow).
* Overall, the intensity of a heart murmur is
not related to the severity of the lesion;
however for some diseases there is a rough
correlation between the intensity of the
murmur and the severity of the lesion such as:
Mitral valve insufficiency Aortic / subaortic
valve stenosis Pulmonic valve stenosis
The intensity of a murmur is graded on a
scale of 1 to 6:
Grade 1 = a very soft, localized murmur
detected only after several minutes of
listening.
Grade 2 = a soft murmur, heard
immediately but localized to a small area.
· Grade 3 = a moderately intense murmur
that is readily detected and detected over
more than one location.
Grade 4 = a moderately intense or loud murmur,
detected over several areas, usually both sides of the
chest, however a precordial thrill is not detected in this
case.
Grade 5 = a loud murmur accompanied by a
precordial
thrill over the point of maximal intensity.
Grade 6 = a very loud murmur accompanied by
a precordial thrill and the murmur is detected when
the stethoscope is pulled slightly off the chest wall.
Murmur Grades
Thrill
Volume
Grade
no
very faint, only heard with optimal
conditions
1/6
no
loud enough to be obvious
2/6
no
louder than grade 2
3/6
yes
louder than grade 3
4/6
yes
heard with the stethoscope partially off the
chest
5/6
yes
heard with the stethoscope completely off
the chest
6/6
** HYPERTENSION
EXAMINATION:.
Inspection - look for signs of secondary
hypertension
(Cushing; s, Acromegaly, Polycythemia,
Chronic Renal Failure)
Take the Blood Pressure (see above for
technique) in arms and legs
Palpate for radiofemoral delay (coarctation) and
radio-radio delay (dissection of aorta)
Examine the Fundi (see endocrine section to note
what the hypertensive changes are)
Examine the rest of CVS system looking for LVF
secondary to hypertension, and look for signs of
coarctation of aorta also palpate and auscultate
the carotids for bruit because hypertension may lead to
damage, dissection, atheromatous change, etc.
4th Heart sound is present if the patient s BP > 180/110
Palpate abdomen for renal and/or adrenal mass
and look for AAA (which is a complication of HT).
Auscultate for renal bruits 2 cm above and lateral to
umbilicus on both sides (note however that most
bruits heard on the left side of the abdomen are from
the splenic artery and are of no significance)
Examine the CNS for previous strokes
Urinalysis also for evidence of renal disease and
Vanylmendallic Acid and Homovanillic acid
(increased in phaechromocytoma)