PULSE K JAI SHANKAR MD DM CONSULTANT CARDIOLOGIST

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PULSE K JAI SHANKAR

MD DM CONSULTANT
CARDIOLOGIST

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PULSE K. JAI SHANKAR MD, DM
CONSULTANT CARDIOLOGIST INSTITUTE OF
CARDIOVASCULAR DISEASES MADRAS
MEDICAL MISSION

PULSE RATE BLOOD

PRESSURE Pulse
palpation Pulse pressure

PULSE DEFINITION: Pulse is the palpability

over peripheral arteries, a pulse wave which is
a transmitted wave from the root of aorta BRADYARRHYTHMIAS DR
along the vessel wall traveling 10 times faster KARTHIGESAN A M
than blood. Blood travels at speed of -. 5 Consultant cardiologist
mt/sec. Pulse travels at speed of - 5 mt/sec. and

MANAGING CHEST PAIN

PULSE WAVE The arterial pulse reXects the
Dr Carl Shakespeare
performance of LV “Mirror of the heart” It is
Consultant Cardiologist
propagated by incompressible blood both
forwards and laterally. The lateral movement
distends the arterial wall and is felt as pulse.

Jai un accident parce que

jai transgress Pourquoi

PULSE - HISTORY HIPPOCRATES – 4 TH

CENTURY BC Thought that arteries are air
ducts GALEN Arteries contain blood & not air.
HEROPHILUS Recognized that arterial pulses
& cardiac pulses were synchronous.
PULSE - HISTORY Nei Ching Su Weri – The
yellow emperors book of medicine. The oldest
book of medicine still existing. It quotes that
chief means of diagnosis than was pulse. It
was palpated for hours in a dozen sites It was
noted whether strong or weak regular or
irregular At that time as watches were not
invented pulse was timed by the physicians
respiratory excursions.

Determinents of Arterial pulse Left Ventricle:

Stroke volume LV contractility Velocity of LV
ejection Aortic Valve : Normal Stenosis
Regurgitation Both stenosis and regurgitation
Arterial system: Compliance or distensibility
Peripheral vascular resistance Aortic run off

BLOOD FLOW LV pressure when it rises above

aortic pressure becomes driving force for
movement of blood into aorta Driving force is
dependent on 1) Contractility 2) Size & shape
of LV 3) Heart rate. This driving force is
opposed by several forces that impede the
Xow 1) Resistance 2) Inertia 3) Compliance
SYSTOLIC UPSTROKE TIME Onset of pulse
wave to its peak Normal range = 90 -160 ms
Brachial artery = 120 ms Acceleration time in
Echo

PULSE WAVE COMPONENTS Percussion wave

is impulse generated by LV ejection Tidal wave
is percussion wave reXected from upper part
of the body Dicrotic wave is reXected from
lower part of the body often recorded but not
palpable Anacrotic notch occurs towards the
end of rapid ejection phase just before max
pressure is reached Incisura Occurs in
Isovolumic relaxation phase prior to aortic
valve closure. Upstroke comes with S 1 Peak
is reached well before S 2
CENTRAL PULSE The central pulse begins
with AV opening and onset of LV ejection The
rapid rising portion of the arterial pressure
curve is termed anacrotic limb (Greek –
upbeat) An anacrotic notch is frequently
recorded on the ascending limb towards the
end of rapid ejection phase. Peak Aortic Xow
velocity occurs slightly earlier than the peak
pressure. The Pulse shows 2 systolic waves
“Percussion wave” and “Tidal wave”

CENTRAL PULSE The descending limb of the

carotid arterial pulse is less steep than the
ascending limb The descending limb is
interrupted by a incisura a sharp downward
deXection in end systole related to isovolumic
relaxation phase The subsequent small
positive “dicrotic wave” is attributed to 1)
Elastic recoil of aorta and AV 2) ReXected
waves from most distal arteries.

ALTERATIONS IN CENTRAL PULSE

PERIPHERALLY Upstroke becomes steeper
Systolic peak becomes higher Anacrotic notch
disappears Systolic upstroke time becomes
shorter (120 msec)

CENTRAL PULSE PERIPHERAL PULSE

ALTERATIONS IN CENTRAL PULSE
PERIPHERALLY Systolic ejection time
becomes more (320 msec) The dicrotic notch
occurs much later Systolic pressure increases
Diastolic pressure & mean pressure decreases

CAUSES FOR CHANGE IN CENTRAL PULSE

CONTOUR WHEN TRANSMITTED
PERIPHERALLY 1)Distortion & damping of
pulse wave components 2) Different rates of
transmission of various components 3)
Differences in distensibility & caliber of
arteries 4) Changes in the vessel wall due to
age & or disease

CHANGES IN PULSE WITH AGING 1) Increase

in the height of tidal wave 2) Increase in the
height of the incisura 3) Systolic upstroke time
is longer 4) Amplitude & duration of dicrotic
wave decreases Normally PW is taller than TW
and TW is not palpable. In old age, diabetes &
arteriosclerosis TW is taller and this is
clinically appreciated as the pulse reaching a
peak in late systole.

PERIPHERAL ACCESSIBLE ARTERIES 1) Head

& Neck 2) Upper Limb 3) Abdomen 4) Lower
Limb 1) Supericial Temporal 2) Carotids 3)
Subclavian 4) Axillary 5) Brachial 6) Radial 7)
Abdominal aorta 8) Femoral 9) Popliteal 10)
Posterior Tibial 11) Dorsalis Pedal
Localization of arteries The CCA terminates at
C 4 level at upper border of thyroid cartilage
The ECA is palpated medial to the
sternocleidomastoid above upper border of
the thyroid cartilage The ICA is palpated
placing a hand in the mouth and palpating the
tonsillar fauces. The subclavian artery is felt in
the posterior triangle. With the shoulder
depressed, pressure is exerted down back and
medially in the angle between
sternocleidomastoid and clavicle.

Localization of arteries Brachial-Palpation of

the right brachial pulse is accomplished with
the thumb of the examiners right hand as the
patients arm lies supinated at his or her side
Axillary- compression against the humerus.

RADIAL For radial pulse palpation the pts hand

should be supinated & comfortably supported.
The examiners thumb or tip of a single inger
preferably the index is applied to the pulse. In
infants palpation of radial pulse has inherent
limitations 1) Radial artery is very small 2)
Padding of subcutaneous fat is more.

EVALUATION OF ARTERIAL PULSE 1) Rate&

rhythm 2) Volume &tension 3) Character 4)
Vessel wall 5) Peripheral pulses Grade the
palpability Brachio or radio- femoral and
brachio-brachial delay Bruit Palpation of
abdominal artery Ocular fundi Allen’s test
GRADING OF PULSES GRADE 0 -absent pulse
+ - feeble ++ - palpable but diminished
compared to other side +++ - normal ++++ -
high volume or bounding pulse

ABNORMAL PULSES 1) Pulsus Parvus 2)

Pulsus Tardus 3) Hypokinetic Pulse 4)
Hyperkinetic Pulse ( Bounding) 5) Brisk or
Jerky Pulse 6) Water Hammer Pulse 7)
Collapsing Pulse 8) Corrigans Pulse 9)
Anacrotic Pulse 10) Bisferrians Pulse 11)
Dicrotic Pulse 12) Pulsus Paradoxsus 13)
Pulsus Alternans 14) Pulsus Bigeminny

PULSUS PARVUS A slow rising pulse Low

volume pulse Best appreciated in carotids
Seen in severe AS and severe heart failure.

PULSUS TARDUS( Anacrotic pulse) Late

peaking Peak is delayed and nearer to S 2
Best appreciated by simultaneous
auscultation of the heart and palpation of
carotid pulse Seen in all forms of ixed
obstruction to the LVOT
ANACROTIC PULSE Pulsus parvus et tardus
with accentuation of the anacrotic notch and a
small volume pulse. Characterized by 1)Slow
upstroke 2)Delayed peak 3)Small volume

CHARACTERISTICS OF ANACROTIC PULSE

1)Pulsus parvus 2)Pulsus tardus 3)Small
volume 4)Prominent anacrotic notch which
appears earlier 5)Dicrotic notch disappears It
is well felt in the carotids Earlier the anacrotic
notch severe the stenosis correlates with a
gradient of 70 mm. Hg

Normal arterial pulse with AS Mild AS

Associated AR HOCM Supravalvular AS, Co. A
In children and elderly

HYPOKINETIC PULSE Small or diminished

pulse 1) Low CO 2) LV Dysfunction 3) CCF 4)
Hypotension 5) LVOT Obstruction In
Hypokinetic pulse Normal upstroke indicates
decreased SV Slow uprise indicates LVOT
obstruction
HYPERKINETIC PULSE 1) Anxiety 6) Alcohol
intake 2) Anaemia 7) Cigarette smoking 3)
Thyrotoxicosis 8) SHT with Atherosclerosis 4)
Exercise 9) Isolated Systolic HT 5) Hot humid
environment

HYPERKINETIC PULSE Hyperkinetic pulse has

a larger than normal amplitude and results
from 1) Increased LV ejection velocity 2)
Increased Stroke volume 3) Increased arterial
pressure.

Mechanisms of high pulse volume Elderly

Atherosclerotic nondistensible arterial system
Emotional excitability, anxiety Increased SV
High cardiac output status Increased SV Low
diastolic pressure Conditions with aortic
runoff Low diastolic pressure Increased SB
Systemic hypertension Nondistensible arterial
system

The arterial pulse in MR Characteristic pulse

Signiicance Normal volume with collapsing
pulse Severe MR with good LV function
Bisferiens pulse MR in association with HOCM
Brockenbrough sign MR in association with
HOCM Slow rising pulse Functional MR with
AS Pulsus alternans Secondary MR with
cardiomyopathy or Myocariditis Irregularly
irregular pulse of AF Rheumatic MR Slow but
regular pulse C-TGA with left AV valve
regurgitation Asymmetry of pulses Infective
endocarditis with systemic embolism
JERKY PULSE Jerky pulse is a pulse with a
brisk or sharp upstroke that literally taps
against the palpating ingers. The pulse
volume is not increased Rapid upstroke /
Normal downstroke / Normal volume Seen
typically in HCM

COLLAPSING OR WATER HAMMER PULSE

Thomas Watson(1844) coined the term after
victorian toy. The collapsing pulse is due to : i)
Diastolic run off into the LV ii) ReXex
vasodilatation mediated by carotid
baroreceptors secondary to large stroke
volume iii) Rapid run off from the periphery
due to decreased systemic vascular
resistance. Best appreciated at the radial
pulse with the palmer side of the examiner’s
hand with the patient’s arm suddenly elevated
above the shoulder. This may be related to the
artery becoming more in the line with the
central aorta, allowing direct systolic ejection
and diastolic backward Xow.

COLLAPSING PULSE With aortic run off: AR,

PDA, AP window, RSOV into right side and AV
istula. Cyanotic CHD : Truncus arteriosus with
truncal run off in to PA or truncal insumciency,
Pulmonary atresia with AP collaterals, TOF
with AP collaterals/associated PDA/
associated AR / after BT shunt. Hyperkinetic
states Pregnancy, Anemia, thyrotoxicosis,
Beriberi, Fever, Paget’s disease of Bone
Normal Volume Collapsing Pulse 1) MR 2)
VSD

PERIPHERAL SIGNS OF AR HEAD & NECK 1)

De Mussets sign 2) Light House Sign 3)
Landolis sign 3) Quinckies sign 4) Mullers
sign 5) Carotid shudder 6) Corrigans Pulse 7)
Julians sign 8) Minervini’s sign 9) Logue’s sign
Head bobbing Alt Xushing & blanching of face
Alteration in pupillary size with cardiac cycle
Capillary pulsation over lips Uvula pulsation
Thrill over carotid during upstroke Visible
carotid pulse of AR Pulsation of retinal
vessels. Strong lingual pulsations. Tongue
depressor moves up and down when tongue is
depressed. Pulsation of sternoclavicular
junction when AR is associated with aortic
dissection.
PERIPHERAL SIGNS OF AR LIMBS 10)
Bisferiens Pulse 11) Locomotor Brachi 12)
Hills sign Double peaked Pulse Dancing
Brachialis LL SBP > 20 mm than UL Mild 20
-40 mmhg Moderate 40 -60 mmhg severe >60
mmhg 13) Pistol shot Femoralis Systolic
sounds over FA 14) Traubes sign Systolic &
Diastolic sounds 15) Durozies murmur. Distal
occlusion diastolic murmur Proximal
occlusion systolic murmur 16) Palfrey’s sign
Pistol shot sound over radial artery

PERIPHERAL SIGNS OF AR ABDOMEN 17)

Rosenbachs sign - Liver Pulsation 18)
Gerhardts sign - Splenic Pulsation 19)
Dennison’s sign - Presence of pulsations in
cervix

Bisferiens pulse Normally percussion wave is

felt but not the tidal wave. In all the conditions
where percussion wave is prominent, tidal
wave also becomes prominent. Mechanism: In
combined AS and AR, the stenotic component
permits a jet, & lateral to the jet there is a fall
in pressure( Bernoulli Phenomenon), this
results in a dip or inward movement in the
pulse with secondary outward movement in a
pulse or tidal wave.

Bisferiens pulse
Bisferiens pulse Normally both waves are
prominent in patients with severe AR. In
HOCM, the initial part of left ventricular
ejection is rapid, resulting in rapid upstroke. As
obstruction to the outXow starts later in the
systole, due to SAM, a sudden interruption to
left ventricular ejection occurs resulting in a
dip in the pressure pulse followed by the slow
rising pulse wave, which is characteristic of
HOCM ( spike and dome pattern). The
percussion wave is more prominent than tidal
wave in HOCM. Seen in Severe AR, AS with AR,
HOCM, hyperkinetic circulatory state, after
exercise

DICROTIC PULSE Dicrotic pulse has an

accentuated dicrotic wave and hence is a
twice beating pulse, one in systole and one in
diastole. Requirements : 1) Hypotension 2)
Reduced Peripheral Vascular Resistance
When the reXection wave travels rapidly and
meets the original wave well in advance, it is
lost in it. In rigid and nondistensible arterial
system, as in SHT, dicrotic pulse in never
present. It is differentiated from the bisferiens
pulse by the simultaneous auscultation of the
heart sounds.

DICROTIC PULSE It is more noticeable in the

beat following a PVC. It is better appreciated
during inspiration or inhalation of amyl nitrite.
IABP-augmented wave due to diastolic Xow
occlusion in descending aorta Rarely present
when BP > 130 mm. Hg and in patients
beyond 50 years of age.

DICROTIC PULSE 1) Healthy young adults 2)

Fever 3) Hypovolemic shock 4) CCF 5) Cardiac
tamponade 6) Sepsis 7) Post AVR 8) IABP
TWICE BEATING PULSE Anacrotic, Bisferiens ,
Dicrotic Differentiation: The double peaking
occurs A) On the upstroke in Anacrotic; late
peaking B) On the peak in Bisferiens- Both in
Systole; rapid rising C) On the downstroke in
Dicrotic ; normal rising One in Systole & One in
Diastole

PULSUS PARADOXUS Paradox about the pulse

is absence of pulse during inspiration but
presence of heart sounds & was coined by
Adolph Kussmaul in 1873. Suspected if the
pulse varies with inspiration in all accessible
arteries. the term paradoxus is that normally
there is a fall in BP during inspiration (4 -6
mm/hg) which in PP is exaggerated (>10
mm/hg) MISNOMER-

PULSUS PARADOXUS LV illing is reduced

during inspiration because exaggerated RV
illing causes 1) Leftward shift of IVS reducing
LV volume & diastolic compliance 2) Elevated
intrapericardial pressure which is transmitted
to the LA but not the extraparenchymal
pulmonary veins and hence a decreased
pulmonary vein – LA pressure gradient
3)Inspiratory pooling of blood in the
pulmonary bed produces decline in LA and LV
illing. [Underilled LV may be operating in the
steep ascending limb of Starling curve so that
any inspiratory reduction of LV illing results in
marked depression of the LV stroke volume
and the systolic pressure].

Pulsus paradoxus
MEASUREMENT To detect pulsus paradoxus
inXate the cuff rapidly above the systolic
pressure and then slowly deXate it. The
difference of the systolic pressure at which
sounds are irst heard only during expiration
and later during both expiration and
inspiration is a measure of the magnitude of
PP.

PULSUS PARADOXUS - CAUSES Physiological

- 1) Obesity 2) Pregnancy RS - 3) Bronchial
Asthma 4) Emphysema 5) COPD 6) Large
Bilateral Pleural effusion

PULSUS PARADOXUS - CAUSES CVS 7)

Cardiac Tamponade 8) Constrictive
Pericarditis (1/3 rd) 9) Hypovolemic shock 10)
Pulmonary embolism 11) RV Infarct 12)
Cardiomyopathy 13) SVC Obstruction 14) Post
Thoracotomy

DETERMINANTS OF PP 1) Venous return 2) LV

afterload 3) Diastolic ventricular
interdependence 4) Lung volume 5)
Circulatory reXexes The principal determinant
is underilling of LV during inspiration in
relation to RV
PULSUS PARADOXUS CARDIAC CAUSE
Inspiratory increase in venous pressure
(Kussmauls sign) RESPIRATORY CAUSE
Expiratory increase in venous pressure.

CARDIAC TAMPONADE WITHOUT PP 1) LVH

2) RVH 3) PHT 4) ASD, VSD 5) AR 6) Regional
Tamponade Mechanism for absence of PP is
lack of competitive ventricular illing during
inspiration.

REVERSED PP In Reversed Pulsus Paradoxus

there is an increase in systemic pressure with
inspiration 1) HOCM : Mechanism unknown.
2) Isorhythmic AV dissociation : Atrial activity
precedes QRS during inspiration and marches
into QRS during expiration. The atrial activity
during inspiration increases the stroke volume
and its lack during expiration decreases the
stroke volume and systolic pressure. 3) IPPV :
Intrathoracic pressure is higher during
inspiration and lower during expiration.

PULSUS ALTERNANS Beats occur at regular

intervals but in which there is a regular
attenuation of the systolic height of the
pressure pulse. It was irst described by
Traube in 1872. Pulsus Alternans is a
peripheral manifestation of LV failure 1)
Alteration in the height of the pressure pulse
2) Alteration in the rate of rise. It is the latter
that is appreciated during palpation.
PULSUS ALTERNANS PA is better felt in distal
vessels than proximal- rate of rise & peak
pressure developed are accentuated during
peripheral transmission of the arterial pulse
pressure. Light pressure is applied to palpate
Pulsus alternans. Mild degree of PA is
detected by sphygmomanometer. InXate the
BP cuff rapidly above SBP and then deXate
slowly until Korotkoffs sounds are audible. At
this point beats are heard at one half of the
heart rate. When the cuff is deXated further
the rate doubles.

PULSUS ALTERNANS - MECHANISM It is due

to alteration of the contractile state of at least
part of the myocardium, caused by failure of
electromechanical coupling in some cells
during weaker contraction. Alternate more and
less number of contractile elements
participate in each contraction. Correlates
with alteration in intensity f Korotkoff sounds.

Types of Pulsus Alternans: Total: When the

weak beat is not percieved at all or when
involving both sides of the heart. Partial: When
invloving only RV ( as in PE) or LV (as in AS).
Concordant alternans: Simultaneous alternans
of right and left ventricles. Discordant
alternans: Alternating alternans of right and
left ventricles.

HOW TO LOOK FOR PA 1) Regular HR 2) Felt in

peripheral arteries 3) Light pressure should be
applied 4) Breath should be held in mid
expiration 5) Can be brought out or
exaggerated by decreasing venous return by
a) Sitting b) Standing c) Head up tilting 6) It is
usually associated with S 3.
PVC, rapid atrial pacing, IVC occlusion,
myocardial ischemia and intracoronary
injection of contrast during coronary
arteriography are known to induce alternans.
By infusion of nitroglycerine, Valsalva
maneuver and in the presence of aortic
regurgitation or systemic hypertension, pulsus
alternans can be exaggerated.

PULSUS ALTERNANS - CAUSES 1. 2. 3. 4. 5. 6.

7. 8. 9. LV Failure of any cause Myocarditis,
DCM Acute pulmonary embolism Severe AS
with failure Severe PS with failure Severe AR
with failure specially after aortic valve
replacement. BrieXy during or after
supraventricular tachycardia Severe systemic
hypertension. Transient right ventricular
outXow occlusion during balloon dilatation of
pulmonary stenosis.

DIFFERENTIATING PA FROM BIGEMINY 1)

Pulsus Alternans is associated with LVS 3 2)
In PA the interval between the weak & strong
beats are equal 3) In Pulsus Bigeminy the
weaker beats arise prematurely and the
stronger beats occur after a pause resulting in
ventricular cycles that are alternatively short
and long.
TIME TAKEN BY AORTIC PULSE WAVE TO
REACH 1) Carotids 2) Brachials 3) Femoral 4)
Radial - 30 ms. - 60 ms. - 75 ms. - 80 ms.

RADIOFEMORAL DELAY It is not the delayed

arrival of the femoral pulse wave but instead a
slow rate of rise to a delayed peak. CAUSES :
Coarctation of Aorta. Occlusive disease of the
bifurcation of the aorta, common iliac or
external iliac arteries. RIGHT RFD-
Supravalvular AS

Co. A WITH ABSENT RFD Co. A + BAV with AS

or AR Co. A with MR Co. A with Supravalvular
AS Pseudo Coarctation.
PULSE DEFICIT Difference between apex beat
and radial pulse > 10 beats/mt occurs in AF
With VPC if they are too weak to open the
aortic valve.

Irregular pulse Irregularly irregular-AF

Regularly irregular- frequent VPC Sinus
arrhythmia-phasic variation in heart rate
a)Respiratory b) Nonrespiratory-digitoxicity

Causes of rapid irregular pulse Atrial

ibrillation Atrial Xutter with varying block
Atrial tachycardia with varying block
Multifocal ventricular tachycardia AF with
WPW syndrome Frequent multifocal atrial and
ventricular ectopy

Causes of Rapid Regular pulse Sinus

tachycardia Supraventricular tachycardia
Paroxysmal atrial tachycardia Junctional
tachycardia Atrial tachycardia with ixed block
Atrial Xutter with ixed block Ventricular
tachycardia
Causes of Bradycardia Sinus bradycardia
Complete heart block High grade heart block
Bigeminal rhythm with impalpable premature
beat Pulsus alternans with impalpable weak
beat

FREQUENT VPC Vs AF VPC – 2 beats in quick

succession followed by a long pause. (Normal
beat followed by premature beat) APC – 2
beats in quick succession followed by a short
pause. AF - Irregular in rate , rhythm & force
Long pause that is not preceded by 2 beats in
quick succession.

UNEQUAL UPPER & LOWER LIMB PULSE

Coarctation of Aorta Aortoarteritis Dissection
of Aorta Atherosclerosis Trauma

UNEQUAL CAROTIDS Aortoarteritis Dissecting

aneurysm of Aorta Atherosclerosis
Thromboembolic occlusion Supravalvular AS
UNEQUAL RADIALS Aortoarteritis Dissecting
aneurysm of Aorta Thromboembolic
obstruction Previous catheterization Cervical
rib Scalenus Anticus syndrome Anomalous Rt
Subclavian artery Aberrant course of Radial
artery Arteritis.

ABSENT FEMORALS Dissecting aneurysm

Coarctation of aorta Pseudoxanthoma
elasticum Hypoplastic External Iliac artery.

Points to remember 1)If the arterial pulse is

regular in a patient with established atrial
ibrillation on digitalis therapy, digitoxicity with
AV nodal rhythm should be considered.
2)Presence of dicrotic wave always suggests
a grave prognosis. 3) Severe MR with good LV
function results in normal volume collapsing
pulse. This is due to rapid ejection by the LV
with the advantage of lesser afterload and
more preload. With the onset of LV
dysfunction, pulse loses its collapsing
character 4)Electrical alternans has no
relationship to pulsus alternans

Report
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