Download CV exam_faz III_OCT2013

CARDIOVASCULAR
EXAMINATION
Assoc Prof Elif Eroğlu Büyüköner
October 2013
EXAMINATION of the
CARDIOVASCULAR SYSTEM
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General inspection
Specific inspection
Pulse
Carotid
Neck veins
Praecordium
Auscultation
Lung bases,liver, ankles
Veins and arteries in the legs
GENERAL INSPECTION
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General build and appearence
Colour
Respiration (abnormal breathing
pattern, shortness of breath)
Signs of distress and response
Conscious level
Myxoedema
Hyperthyroidism
Mitral Facies / Facies
Mitralis
Ear Lobe Crease
Down Syndrome
Moonface
Acromegaly
SPECIFIC INSPECTION
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Cyanosis
– Central: mucous membranes-tongue
– Peripheral: extremities
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Clubbing
Anemia
Edema
Peripheral perfusion
Body habitus
Specific signs of cardiac pathologies: IE stigmata,
arcus senilis, xanthome and xanthelasma
CYANOSIS and CLUBBING
Central Cyanosis
Peripheral Cyanosis
Icterus
Petechiae
Erythema Marginatum
Signs of atherosclerosis
Xanthelesma
Arcus juvenilis
Sign of premature atherosclerosis
xanthoma
Xantoma
IE/specific signs
Body habitus: Marfan
syndrome, thorax
abnormalities
The PULSE
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Rate
– Normal sinus 60-100bpm
– Sinus bradycardia <60 bpm
– Sinus tachycardia >100 bpm
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Regularity
– Sinus arrhytmia: varies with respiration
– Intermittant irregularity: ectopic beats
– Continously irregular: atrial fibrillation
Carotid examination
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Carotid upstroke
– Brisk/normal/delaye
d
– Volume:increased/n
ormal/decreased
– Anacrotic/bisferiens
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Carotid auscultation
– Bruit
– Transmitted
murmur
– A2 audible in the
neck
Carotid pulse contour
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A. Hyperkinetic:AR
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B.Bisferiens: AS/AR
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C.Bifid: IHSS
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D.Hypokinetic/alterna
ns: LVD
E.Parvus et tardus:
AS
BLOOD PRESSURE
MEASUREMENT
Recommended technique
for BP measurement
Juguler venous pulse
Patient position for JVP
assessment
JVP measurement
Jugular Venous Pressure
Waveform
Normal JVP waves and
descents
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a wave - atrial systole
x descent – onset of
atrial relaxation
c wave - small positive
notch in the 'x' descent
due to bulging of the
AV ring into the atria in
ventricular contraction.
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x' (prime) descent !!!
– occurs during systole due to RV
contraction pulling down the
TV valve ring “descent of the
base”
– a measure of RV contractility
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v wave - after the x' descent - slow
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y descent - rapid emptying of the
positive wave due to right atrial filling
from venous return
RA into RV due to TV opening
Abnormal “a” wave
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AV valve obstruction: TS, RA myxoma
Decreased RV compliance:RVH, PS,
PHT
AV dysassociation:AV blocks, “Cannon”
a waves
Severe HCM: Bernheim effect
No visible “a” wave in AF
X’ descent
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Beginning of the RA diastole, before venous
filling to the RA, during RV systole. RVFW
moves to the septum, TV moves to the apex
and RA base is pulled down (RA pressure
falls)
More prominent during inspiration
Increases with RV contractility:tamponade
RV volume inc: ASD, VSD
RV pressure inc: PD, PHT
Decreases in RV contractility: reduced x’
v wave
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RA filling, together with S2
Severe TR: CV fusion, no X’ descent
y descent
• RV filling (early diastole)
• Inc: TR, CP, RCM
• Dec: Tamponade, TS
Apical Impulse:
Visualization
to assess ventricular size/thickness
Normally distinct and located at 4ICS at/inside the midclavicular line
Apical Impulse
(abnormal):
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Hyperdynamic impulse in normal
location: think increased cardiac
output or LVH
Hyperdynamic and
downward/leftwardly displaced: think
LVE
Indistinct impulse associated with RVH
Precordial heave is seen with RVE
Thrills:
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Palpation of a loud murmur
Found in the precordial, suprasternal,
or carotid artery area
If low intensity murmur, probably just
a pulsation and NOT a thrill
Auscultation
Heart Sounds
S1 (cont.):
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If split heard better at the apex, may
actually be S4 or ejection click
Tends to be more low-pitched and
long as compared to S2
Differentiate S1 from S2 by palpating
carotid pulse:
 S1 comes before and S2 comes after
carotid upstroke
Decreased S1:
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Slowed ventricular
ejection
rate/volume
Mitral insufficiency
Increased chest
wall thickness
Pericardial effusion
Hypothyroidism
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Cardiomyopathy
LBBB
Shock
Aortic insufficiency
First degree AV
block
Other Abnormal S1
(cont.):
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Increased S1:
 Increased cardiac output
 Increased A-V valve flow velocity (mitral
stenosis)
S2:
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From closure vibrations of aortic and
pulmonary valves
Divided into A2 and P2 (aortic and
pulmonary closure sounds)
Best heard at LMSB/2LICS
Higher pitched than S1/better heard
with diaphragm
S2 splitting (normal):
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Normally split due to different
impedance of systemic and pulmonary
vascular beds
Audible split with > 20 msec
difference
Split in 2/3 of newborns by 16 hrs. of
age, 80% by 48 hours
Harder to discern in heart rates > 100
bpm
S2 splitting (normal,
cont.):
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Respiratory variation causes  splitting
on inspiration:  pulmonary vascular
resistance
When supine, slight splitting can occur
in expiration
When upright, S2 usually becomes
single with expiration
S2 splitting (abnormal,
cont.):
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Fixed splitting
 ASD
S2 splitting (abnormal,
cont.):
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Wide /mobile
splitting
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Mild PS
RVOTO
Large VSD or PDA
Idiopathic PA
dilation
 Severe MR
 RBBB
 PVC’s
S2 splitting (abnormal,
cont.):
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Reversed splitting
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LBBB
WPW
Paced beats
PVC’s
AS
PDA
LV failure
Extra heart sounds
S3 (gallop):
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Usually physiologic
Low pitched sound, occurs with rapid
filling of ventricles in early diastole
Due to sudden intrinsic limitation of
longitudinal expansion of ventricular
wall
S3 (cont.):
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Best heard with patient supine or in
left lateral decubitus
Increased by exercise, abdominal
pressure, or lifting legs
LV S3 heard at apex and RV S3 heard
at LLSB
S3 (abnormal):
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Seen in HF, severe MR--disappears
after treatment
S4 (gallop):
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Nearly always pathologic
Can be normal in elderly or athletes
Low pitched sound in late diastole
Due to elevated LVEDP (poor
compliance) causing vibrations in stiff
ventricular myocardium as it fills
S4 (cont.):
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Better heard at the apex or LLSB in
the supine or left lateral decubitus
position
Occurs separate from S3 or as
summation gallop (single intense
diastolic sound) with S3
S4 Associations:
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CHF!!!
HCM
severe systemic HTN
pulmonary HTN
Ebstein’s anomaly
myocarditis
S4 Associations (cont.):
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Tricuspid atresia
TAPVR
CoA
AS
Kawasaki’s disease
Ejection clicks
Timing of Heart Sounds
Cardiac murmurs
Basic Pathophysiology
Systolic
Diastolic
Describing a heart murmur
1. Timing
– murmurs are longer than heart sounds
– HS can distinguished by simultaneous palpation of
the carotid arterial pulse
– systolic, diastolic, continuous
2. Shape
– crescendo (grows louder), decrescendo, crescendodecrescendo, plateau
3. Location of maximum intensity
– is determined by the site where the murmur originates
– e.g. A, P, T, M listening areas
Describing a heart murmur
con’t:
4. Radiation
– reflects the intensity of the murmur and the direction
of blood flow
5. Intensity
– graded on a 6 point scale
Grade 1 = very faint
 Grade 2 = quiet but heard immediately
 Grade 3 = moderately loud
 Grade 4 = loud
 Grade 5 = heard with stethoscope partly off the chest
 Grade 6 = no stethoscope needed
*Note: Thrills are assoc. with murmurs of grades 4 - 6
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Describing a heart murmur
con’t:
6. Pitch
– high, medium, low
7. Quality
– blowing, harsh, rumbling, and musical
8. Others:
i. Variation with respiration
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Right sided murmurs change more than left sided
ii. Variation with position of the patient
iii. Variation with special maneuvers
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Valsalva/Standing => Murmurs decrease in length and intensity
EXCEPT: Hypertrophic cardiomyopathy and Mitral valve
prolapse
Systolic Murmurs
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Derived from increased turbulence associated
with:
1. Increased flow across normal SL valve or into a
dilated great vessel
2. Flow across an abnormal SL valve or narrowed
ventricular outflow tract - e.g. aortic stenosis
3. Flow across an incompetent AV valve - e.g. mitral
regurg.
4. Flow across the interventricular septum
Systolic Murmurs
Early Systolic murmurs
1. Acute severe mitral regurgitation
– decrescendo murmur
– best heard at apical impulse
– Caused by:
i. Papillary muscle rupture
ii. Infective endocarditis
iii. Rupture of the chordae tendineae
iv. Blunt chest wall trauma
2. Congenital, small muscular septal defect
3. Tricuspid regurg. with normal PA pressures
Midsystolic (ejection)
murmurs
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Are the most common kind of heart murmur
Are usually crescendo-decrescendo
They may be:
1. Innocent
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common in children and young adults
2. Physiologic
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can be detected in hyperdynamic states
e.g. anemia, pregnancy, fever, and hyperthyroidism
3. Pathologic
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are secondary to structural CV abnormalities
e.g. Aortic stenosis, Hypertrophic cardiomyopathy, Pulmonic
stenosis
Pansystolic (Holosystolic)
Murmurs
Are pathologic
 Murmur begins immediately with S1 and continues up to
S2
1. Mitral valve regurgitation
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– Loudest at the left ventricular apex
– Radiation reflects the direction of the regurgitant jet
i. To the base of the heart = anterosuperior jet (flail posterior
leaflet)
ii. To the axilla and back = posterior jet (flail anterior leaflet
– Also usually associated with a systolic thrill, a soft S3, and a short
diastolic rumbling (best heard in left lateral decubitus
2. Tricuspid valve regurgitation
3. Ventricular septal defect
Diastolic Murmurs
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Almost always indicate heart disease
Two basic types:
1. Early decrescendo diastolic murmurs
– signify regurgitant flow through an imcompetent semilunar
valve
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e.g. aortic regurgitation
2. Rumbling diastolic murmurs in mid- or late diastole
– suggest stenosis of an AV valve
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e.g. mitral stenosis
Diastolic Murmurs
Continuous Murmurs
Begin in systole, peak near s2, and continue into all or
part of diastole.
1. Cervical venous hum
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– Audible in kids; can be abolished by compression over the IJV
2. Mammary souffle
– Represents augmented arterial flow through engorged breasts
– Becomes audible during late 3rd trimester and lactation
3. Patent Ductus Arteriosus
– Has a harsh, machinery-like quality
4. Pericardial friction rub
– Has scratchy, scraping quality
Back to the Basics
1. When does it occur - systole or diastole
2. Where is it loudest - A, P, T, M
I. Systolic Murmurs:
1. Aortic stenosis - ejection type
2. Mitral regurgitation - holosystolic
3. Mitral valve prolapse - late systole
II. Diastolic Murmurs:
1. Aortic regurgitation - early diastole
2. Mitral stenosis - mid to late diastole
SUMMARY
A. Presystolic murmur
– Mitral/Tricuspid stenosis
B. Mitral/Tricuspid regurg.
C. Aortic ejection murmur
D. Pulmonic stenosis (spilling
through S20
E. Aortic/Pulm. diastolic
murmur
F. Mitral stenosis w/ Opening
snap
G. Mid-diastolic inflow murmur
H. Continuous murmur of PDA
Summary
Innocent murmurs
Characteristics of
Pathologic Murmurs
Signs and symptoms of
cardiovascular diseases
Common Cardiac Symptoms
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Chest Pain
Dyspnoea
Tachycardia
Fatigue
Syncope
Dizziness
Cyanosis
Oedema
Cough
Haemoptysis
Appetite & weight loss
Hoarseness
Nausea & Vomiting
Nocturia
Chest Pain
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Localization
Radiation
Character
Duration
Precipitating factors
Alleviating factors
Accompanying findings
Dyspnea
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The sensation of breathlessness or
inadequate breathing.
Most common complaint of patients
with cardiopulmonary diseases
Shortness of breath, breathlessness
Uncomfortable/abnormal breathing
Dyspnea
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Hyperventilation: Increase in
respiratuary workload
– Hypoxemia
– Hypercapnia
– Acidosis
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Hypoventilation:Decrease in ventilation
capacity
– COPD
Cyanosis
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Cyanosis is a bluish or purplish tinge
to the skin and mucous membranes.
Approximately 5 g/dL of unoxygenated
hemoglobin in the capillaries
generates the dark blue color
appreciated clinically as cyanosis
Peripheral cyanosis
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Peripheral cyanosis is a dusky or bluish
tinge to the fingers and toes and may
occur with or without central cyanosis
(ie, with or without hypoxemia).
When unaccompanied by hypoxemia,
as determined by blood gas analysis,
peripheral cyanosis is caused by
peripheral vasoconstriction
Causes
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All common causes of central cyanosis
Arterial obstruction
Cold exposure (due to vasoconstriction)
Raynaud's phenomenon (vasoconstriction)
Reduced cardiac output (e.g. heart failure,
hypovolaemia)
Vasoconstriction
Venous obstruction (e.g. deep vein
thrombosis)
Central cyanosis
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Central cyanosis is often due to a
circulatory or ventilatory problem that
leads to poor blood oxygenation in the
lungs or greater oxygen extraction due
to slowing down of blood circulation in
the skin's blood vessels.
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1.
Central Nervous System:
– Intracranial hemorrhage
– Cerebral anoxia
– Drug overdose (e.g. Heroin )
2. Respiratory System:
– Bronchiolitis
– Bronchospasm (e.g. Asthma)
– Lung disease
– Pulmonary embolism
– Hypoventilation
3.Cardiac Disorders:
– Congenital heart disease (e.g. Tetralogy of Fallot, Right to left shunts in
heart or great vessels)
– Heart failure
– Heart valve disease
– Myocardial infarction
4.Blood:
– Methemoglobinemia
– Polycythaemia
5.Others:
– High altitude
– Hypothermia
– Congenital cyanosis
Differential cyanosis
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Differential cyanosis, meaning
cyanosis and clubbing of the lower
extremities with normal upper
extremity nailbeds, is diagnostic of
patent ductus arteriosus with
pulmonary hypertension
Differential cyanosis
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Desaturated blood from the ductus enters
the aorta distal to the left subclavian artery,
sparing the brachiocephalic circulation. The
oral mucosa and tongue receive saturated
blood and are not cyanotic. In some cases,
ductal flow will enter the left subclavian
artery and cause clubbing of the left hand
as well as the feet.
Differential Diagnosis of Chest Pain /
Göğüs Ağrısının Ayırıcı Tanısı
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Nonkardiyak intratorasik dokular
/ Noncardiac intrathorasic tissues
Boyun & “göğüs duvarı” dokuları
/ Neck & “chest wall” tissues
Subdiafragmatik organlar
/ Subdiaphragmatic organs
Differential Diagnosis of Dyspnoea
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Cardiac
Pulmonary
Chest wall abnormalities
Anemia
Obesity
Hypoxia
Physicogenic
Central nervous system
Cardiac Dyspnoea
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Exertional Dyspnoea
Orthopnoea
Paroxysmal nocturnal dyspnoea
Pulmonary oedema
Cheyne-Stokes ventilation
Systemic Diseases that may lead to Heart Diseases
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Endocrine System Diseases
Collagen Tissue Disorders
Haematologic Diseases
Metabolic Disorders
Infectious Diseases
Chromosome Abnormalities
Malign Disorders
Muscle Diseases