By Ragab abd elsalam ( MD) Prof. of Cardiology. Clinical Cardiology OV erview. 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
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
(1) Recurrent chest pain:
- 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.
-Pain is usually described as sharp or burning and reproduced by local pressure.
- 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.
- 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.
-The cause of pain may be:
-Right ventricular ischemia
- Enlarged right ventricle & pulmonary artery may compress on chest &sternum.
Prolonged chest pain
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.
> Exertional dyspnea.
> Nausea, indigestion.
> Dizziness, sweating.
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.
It can be divided into three subsets:
It is the patient complaint of:
- shortness of breath.
or- he can’t get enough breath.
or- awareness of respiration.
- Dyspnea on effort (exertional dyspnea).
- Paroxysmal nocturnal dyspnea.
- Acute pulmonary edema.
- Cheyne-Stokes Breathing.
- Dry non-productive cough.
Pregnancy “huff and puff”
Compansatory hyperpnea associated with metabolic acidosis due to diabetes mellitus and uremia.
- What is about the daily activity of the patient?
- When the patient began to notice increasing dyspnea?
*When dyspnea is associated with wheezing:
It implies that the patient has more dyspnea when he is lying down.
Ask the patient:
(c) paroxysmal Nocturnal Dyspnea:
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.
Periods of hyperpnea which alternate with periods of apnea.
This type of breathing occurs in:
Dyspnea that occurs in only one of several recombent positions not due to congestive heart failure:
It is the dyspnea provoked by sitting-up.
Paroxysmal Nocturnal dyspnea (PND).
Patients with severe pulmonary hypertension associated with atrial septal defect, or patent ductus arteriosus, may have hemoptysis, secondary to rupture of pulmonary capillaries.
* Clinical significance of history of cyanosis:
- tricuspid atresia.
But the patient seldom complains of cyanosis in these problems.
(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.
Syncopethat 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.
*Common causes include:
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.
Significance Of The History As a pointer to the Diagnosis
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.
It is characterized by
It is characterized by:
* It is observed in patients with:
It is the bobbing motion of the head, synchronous with hear tbeat.
It is characterized by:
may lead to infected emboli.
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.
It has a specific physiologic implication:
C = Cyanotic heart diseases
L = Lung diseases
U = Ulcerative colitis , Crohn,s diseases
B= Birth defect .
I = Infective endocardits
N = Neoplasm ( es. Hodgkins)
G= Gastrointestinal malapsorption.
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 , Blue-red 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
Involves primarily the trunk and it is characterized by:
** Central obesity is more common in men, while peripheral obesity is more common in women.
According to old standards:
Revised guideline:Any one with BMI 25 is considered abnormal
- It is a granulomatous disease of unknown cause.
(a)Skin is highly sensitive to sunlight:
It is a connective tissue disease.
Excessive iron that deposits in tissues can cause cirrhosis, diabetes mellitus, artheritis, hypogonadism and cardiomyopathy.
(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 Marfans Syndrome,
Downs Syndrome, Turners Syndrome (each of
which has cardiovascular sequelae).
(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 youwill grow accustomed to as a medical student) and inspect the hands of the patient, you may askthe 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
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 indexfingers 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 patients have a diamond shaped space between the two nails, however in patients
of angle can be pronounced.
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.
of lipid in tendons which occurs in Type II Hyperlipidemia
(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
.-Oslers nodes - (O is for Osler as O is for Ouch) – theseare painful red raised nodules on the pads of the fingersand/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
or knee joints) both indicate Type III Hyperlipidemia
(increase in VLDL)
* Examination of the Face:
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 withhypercholesterolemia. However, if it it occurs in the elderly > 65yrs old, then it is insignificant.
*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.
* Xanthelasmawhich are yellow lipid deposits around the eyes
and which occur in type II or type III
* Look for blood vessels on the iris of the patient (called Rubeosis)and it occurs in poorly controlled
patients (it occurs due to high levels of blood glucose being converted to sorbitol by aldose reductase in the eye which deposits as cataracts
** Taking of the Pulse
It is important to turn the patientshand palm side up fortaking the pulse, or else the exainer will not be able toview 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
or Sinus arrhythmia which is increased pulse on inspiration due to increased venous return,and decreased pulse on expiration (it is normal).
@Assess the characterof 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
(ii) Slow Rising Plateau Pulse: This is a
pulse that has a slow rising bolus under your finger, but thenthe 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
@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 causea dramatic increase
>This will feel like a loud pulse under the examiners fingers.
a large arterial occlusion by large atherosclerotic plaque or aneurysmal process
of deoxyhemoglobin in the blood.
patients with anaemia to reach this concentration
of deoxyhemoglobin and so more difficult for them to become centrally cyanosed,
Look at the tongue and note any enlargement which may occur due to amyloidosis (amyloidosis can cause restrictive cardiomyopathy).
(7) Examination of the Neck:
Inspect the neck area for carotid
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:
-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.
Abnormalities of Arterial Pulse:
The size of the arterial pulse is determined by:
-Left ventricular stroke volume.
-Rate of ejection.
-Distensibility of the systemic arterial bed.
-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.
- Shock, tachycardia...).
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
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.
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.
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).
The low output state following open heart surgery, especially aortic valve replacement.
Exaggeration of anacrotic notch gives palpable two wave during systole as in aortic stenosis (Severe).
Pulsus Bisferiens: Bis = twice & feriens = beating:
Causes and Mechanisms
> 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.
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).
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
Sudden critical change in diastolic filling period.
Alternation in the number of cardiac fibres contributing to each systole.
- 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.
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.
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.
*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.
.. Nowposition 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
=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.
> 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)
> 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 vertibro-basilar insufficiency and the blood pressure is lower in one arm than other.
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 (
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.
> Itis 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.
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.
the right JVP is actually closer to the right atrium and so functions
as a more accurate manometer of right atrial pressures).
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 somepeople are purists, and so they consider the right atrium as 0cm.
* Character of the JVP - The wave form of the JVP is complex and you will not be expected tocomment on subtle changes in
these wave forms in different
* But you will be expected
to know the normal wave form
and some pathological manifestations.
Technique A: Jugular Venous
Pressure Measurement (JVP)
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.
> 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
It is a brief positive wave that interruptes the descent of venous pulse from the summit of (a-wave).
> 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.
> 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.
> Downward displacement of the base of the ventricles including TV during ventricular Systole fall in RA pressure.
> Continued atrial Relaxation.
* (Y- wave) = Diastolic collapse:
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
points: ASK ME:• 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.
Absent a-wave in atrial fibrillation due to absent atrial contraction.
Decreased or obliterated X-descent or even systolic expansion.
The predominant wave is Y-descent.
Irregularity of the pulsations.
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
Occurs when the RA contracts against closed TV during RV systoleSo the resulting wave is the fusion of (a,c & v) waves.
> Regular connon waves:
> 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.
Abnormalities of the systolic collapse (x-wave):
In tricuspid regurgitation this collapse may be:
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 Y-descent.
X-descent is shallow.
N.B : X-descent may be prominent & deep than Y-descent if it is associated with active pericaiditis.
Abnormalities of the diastolic collapse (Y-wave).
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.
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 :
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.
- Bronchogenic carcinoma.
- Retrosternal hugely enlarged thyroid gland.
Causes of elevated JVP
- Fluid overload [esp. IV infusion]
- Constrictive pericarditis
- Pericardial effusion
- SVC obstruction
- Tricuspid stenosis or regurgitation
- Hyperdynamic circulation
- Raised Intra-thoracic pressure:
> Pleural Effusion
> Increased Blood volume:
> Acute nephritis.
> Large IV infusion.
- High output states as in:
> Arterio-vnous fistula.
*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.
> 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 X-descent and deep Y descent, when the restriction occurs only after the opening of tricuspid valve.
* Effusive -constrictive pericarditis: the X-descent 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).
-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.
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.
* Presystolic impulse is commonly observed in HOCM, more than aortic stenosis... How?
(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 childrendenotes 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.
- 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).
- 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 right-sided aortic arch.
b) Aortic dissection or aneurysm.
c) Aneurysmally dilated RA & RV.
*Auscultate the Carotid arteries for any bruits.
It is important to know physically why a bruit is
produced in any artery.
* Thereis an equation from physics which describes the
parameters necessary to produce a bruit.
* In effect a bruit is the sound made from turbulent flow.
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:
-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 (secondaryto a reductionin pulmonary function).
>Apex beat: always begin your palpation
of the apex beat from the axillae towards the
> Once you can palpate it (the size of a
2 euro coin)count dow the number of
spaces with the left handwhile
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 apexbeat is 5thintercostal space on the left, and 1 cm medial to
> If the apex beatis 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 beatwhich is indicative of left ventricular failure (LVF).
** Therefore, the size of the apex beat is larger than the normal 2 euro size.
Tapping Apex - A palpable S1 (mitral or tricuspid stenosis)
with a normal apex beat which follows.
The S1 is palpablein 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 youfinally close it....its gonna slam shut.....same idea here).
Parasternal Heave - felt left of sternum
fingers in the intercostal spaces and feel for any heaves)
this is indicative of Right Ventricular Enlargement or
Severe Left Atrial Enlargement
Hunt for a Murmur
-(always listen for HS I and II while listening in all the areas)
-Firstplace the bell of your stethoscope over the mitral area
-Rememberto apply the bell of your stethoscope to the chest wall very lightly or else a diaphragm is created bythe stretched skin and this defeats the purpose of usingthe bell
-Next place the diaphragm at the pulmonary area
(2nd intercostal space, left sternal edge) and auscultate
-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,
carotid pulse todetermine if the murmur is systolic
* 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 pressureand high volume flow).
* Loud A2 = if there is systemic hypertension or aortic stenosis
*Loud P2 = in pulmonary hypertension
*Soft A2 or P2 = Aortic (pulmonary) regurgitation or calcification
** 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.
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 thePVis 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.
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 pressuresand volumes and thus inability for changein volume to occur on inspiration.
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).
atria are contracting appropriately, as a result dont say
that you can hear the S3 sound right after saying that the
patient has Atrial Fibrillation, because this is impossible.
S3: a low pitched sound arises from the l or Rventricles. 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
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 alwayspathological 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 duringangina or MI).
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 pulmonarystenosis (due specifically to bicuspid congenitalvalves)
are redundant mitral valve leaflets or an ASD
them because they are tissue!
* 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.
that begins during or immediately after S1 and ends with the onset of S2
- 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
-My be early diastolic , mid0diastolic
or late ( presystolic) murmurs.
-Typically associated with a PDA, but also arteriovenous
-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
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.
detected over several areas, usually both sides of the
chest, however a precordial thrill is not detected in this case.
thrill over the point of maximal intensity.
a precordial thrill and the murmur is detected when
the stethoscope is pulled slightly off the chest wall.
** 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
radio-radio delay (dissection of aorta)