PE OF DIFFERENT HEART

DISEASES

ARTHUR R. PITARGUE , MD, FPCP, FPCC

ANATOMY
CIRCULATION
AUSCULTATION SITES
AUSCULTATION SITES
APICAL BEAT / IMPULSE
APEX BEAT
Palpation
Palpation
Left Sided Lesions ( i.e. mitral ) / Female /
Obese patients
Aortic Regurgitation /
Pericardial effusion
VALVULAR AND RHD
RHEUMATIC HEART DISEASE
VALVES INVOLVED %
Mitral valve alone 50
Mitral and aortic valves 40
Mitral, aortic and tricuspid 5
Aortic valve 2
All other combinations 3
 MITRAL STENOSIS
• 2/3 are females
• Generally rheumatic in origin ;congenital (rare )
• Diffusely thickened valve leaflets with fibrous
thickening and / or calcific deposits
• Mitral commisures fuse , chordae tendinae fuse
and shorten , valvular cusps become rigid
leading to narrowing of the apex of the funnel
shaped valve
MITRAL VALVE ANATOMY
and STENOSIS
 MITRAL STENOSIS
• Chronic : TR , PR , RV failure
• Symptoms : 2nd to 4th decade ( MVA < 1 cm2)
• Permanent atrial fibrillation – marks turning
point ant its assoc. with acceleration of the rate
at which symptoms progress
• Hemoptysis : rupture of - bronchial venous
connections due to pulmo. venous HPN
• Hoarseness of voice due to dilated left atrium
impinging the left recurrent laryngeal nerve
( Ortner’s Syndrome )
• Dysphagia – LA impinging the esophagus
 MITRAL STENOSIS
PE :
• Peripheral and facial cyanosis , malar rash
pinched and blue fascie
• Prominent “a” waves ( JVP ) due to
vigorous R atrial systole ( sinus rhythm )
• Disappearance of the “ a wave “ thus only “
c - v “ wave during systole ( atrial
fibrillation )
• Right ventricular tap ( RVH ) ; palpable and
prominent “ P2 “
 MITRAL STENOSIS
1.Loud S1 ( first heart sound )
2.Opening snap readily audible in expiration at the
apex but may also be heard at the L sternal edge
of the base of the heart
• Interval of A2 – OS varies invariably with the
severity of MS ; longer duration of the rumble
correlates with the severity of the MS
• Intensities of OS and S1 correlate with the mobility
of the AMVL ( louder more mobile )
3.Diastolic rumble at the apex esp. at the left lateral
decubitus
4.Presystolic murmur ( if sinus rhythm ) due to
vigorous atrial contraction
 MITRAL REGURGITATION
• Incomplete systolic closure of the MV
• More frequent in males
• 1 / 3 due to chronic RHD
• Marked LV enlargement causes dilatation of
the mitral annulus and lateral displacement
of the papillary m. interfere with coaptation
of the valve leaflets
 MITRAL REGURGITATION
SYMPTOMS :
• Fatigue , exertional dyspnea and orthopnea
( a fraction of chronic MR )
• Hemoptysis and systemic embolism ( less
frequently compared to MS )
• Right sided heart failure , w/ painful hepatic
congestion , ankle edema , distended neck
veins, ascites and TR
• ACUTE SEVERE MR : LV failure w/ acute
pulmo. edema and/ or cardiovascular
collapse
 MITRAL REGURGITATION
• Congenital :
1) defect in the endocardial cushion
2) corrected transposition
3) endocardial fibroelastosis
4) parachute mitral valve deformity
• Fibrosis of a papillary muscle ( myocardial
infarction) as well as ventricular aneurysm
involving the base of the papillary muscle
• Transient MR - ischemia
 MITRAL REGURGITATION
PE
• Arterial pressure is usually normal ; severe MR = sharp upstroke
• Prominent “ a “ wave ( JVP ) ; prominent “v “ waves with severe
TR
• Systolic thrill at the apex, hyperdynamic LV w/ brisk systolic
impulse ; AB displaced laterally
• LA enlargement – extend anteriorly and resemble RV lift
• Rocking motion of the chest = combination of retraction of LV
and expansion of the LA during systole
• RV tap = pulmo HPN
 MITRAL REGURGITATION

PE
• absent or soft S1; AV may close prematurely
( wide split S2)
• S3 and / or S4
• HSM or decrescendo type that radiates to the
axilla or to the back ; Carey- Coomb’s murmur
– acute rheumatic fever
• “ Cooing “ or “ sea gull “ - ruptured chordae
tendinae ; musical
 MITRAL VALVE PROLAPSE
• Systolic click – murmur synd. , Barlow’s synd. , Floppy
valve synd. And Billowing mitral leaflet synd .
• excessive or redundant mitral leaflet tissue ( myxomatous
degeneration ) ; increased acid mucopolysaccharide
• Marfan’s syndrome or cystic medial necrosis
• Posterior leaflet is commonly affected & MV annulus is
sometimes enlarged
• elongated chordae tendinae cause or contribute to
regurgitation
• genetically determined collagen tissue disorder
• assoc. w/ thoracic skeletal deformities
• Sequel of acute RF, in chronic RHD and ff’ing mitral
valvulotomy, in ischemic heart dse, and cardiomyopathies,
20% of ostium secundum ASD
 MITRAL VALVE PROLAPSE
PE :
• Mid or late ( nonejection ) systolic click after the S1
due to sudden tensing of slack, elongated chordae
tendinae or by prolapsing mitral lealfet
• Ff’ed by high pitched or late systolic crescendo-
decrescendo murmur, occasionally “ whooping” or
honking “ at the apex
• Click or murmur occur earlier with standing &
Valsalva which decrease left ventricular volume,
diminish the propensity of the MV to prolapse
• Click or murmur delayed or disappear during
squatting and isometric exercise
 AORTIC STENOSIS
SYMPTOMS :
• Valve orifice narrowed to 1/ 2 of normal
• Fifth to seventh decade
• Three cardinal symptom : exertional dyspnea ,
angina pectoris , and syncope
• Orthopnea , PND and pulmo. edema seen in
advance stages
• Usually preterminal findings : RV failure ,
systemic venous HPN , hepatomegaly, AF and
TR
PE :
AORTIC STENOSIS
• Normal systemic arterial pressure ( initial )

Systolic pressure and narrow pulse pressure

• Systemic HPN is unusual ( marked AS )
• Peripheral arterial pulse ( carotid/ brachial ) :
“ pulsus parvus et tardus “
• “ a “ wave may be accentuated ( JVP )
• AB displaced inferiorly and laterally ( LVH )
• Double apical impulse in the left lateral decubitus : systolic
thrill in the base of the heart
• Early systolic ejection sound ( cong. noncalcific AS )
• Paradoxic splitting of the S2
• Ejection systolic murmur best heard at the base transmitted
to the jugular notch and upward along the carotid arteries
• Gallavardin sound : apex ; musical ; systolic murmur
 AORTIC REGURGITATION
• 3/ 4 are males ( pure or predominant AR )
• Females predominate : AR w/ MV dse.
ETIOLOGIES :
• Rheumatic ( 2/ 3 ) less common in pure AR
• Acute AR - due to infective endocarditis
• Discrete membranous subaortic stenosis or cong. bicuspid aortic
valve
• VSD
• Cong. fenestration of the AV
• Trauma ( non penetrating cardiac injuries )
• Dilatation of the aortic annulus ( syphilis and ankylosing
spondylitis)
• Cystic medial necrosis of the ascending aorta
• Idiopathic dilatation
• Severe HPN
• Aortic dissection
 AORTIC REGURGITATION
• Backward flow of blood into the left ventricle due to
failure of coaptation of the aortic valve leaflets ( valvar
or aortic root disease )

ETIOLOGIES
• Cong. Bicuspid AV ; RHD : scarring of the leaflets
causing AS or AR or combination
• Aortic root pathology with minimal valvar pathology :
tertiary syphilis, Marfan’s syndrome , cystic medical
necrosis , ankylosing spondylitis , dissecting
aneurysm
CHRONIC AORTIC REGURGITATION
• Compensated , LV dilatation , increase in
compliance, normal or increased SV
• “ Cor bovinum “ - large heart
• Earliest symptoms : increased pounding sensation
( wide pulse pressure ) with systolic HPN ( increased
SV & aortic diastolic runoff )
• PND & orthopnea : supine position  increase
venous return & resting bradycardia  overload
LV
• Chest pain : decrease coro. bld. flow due to
decrease DBP & increase LVEDP ( severe or poorly
tolerated AR )
 PE OF CHRONIC AORTIC REGURGITATION
• De Musset sign : head bobbing ; dramatic carotid
pulsations
• Quincke’s pulse : capillary pulsation of the nailbeds if light
is shone on the fingertips or glass slide placed over the lips
• Corrigan’s water Hammer pulse / pulsus magnus - strong
arterial pulse
• Traube’s Sign – double sound heard over the femoral artery
during systole
• Pistol shot sound – loud systolic murmur heard over the
femoral arteries
• Duroziez’s sign : systolic murmur heard if the the fem. A. is
partially occluded proximal to the stet and diastolic murmur
heard if the fem a. is partially occluded distal to the stet
• Hill’s sign : popliteal SBP > brachial SBP ( > 60 mm Hg )
PE OF CHRONIC AORTIC REGURGITATION (con’t)

• Becker’s sign : retinal arteriolar pulsations

• Gerhardt’s sign : pulsation of the spleen
• Rosenbuck’s sign : pulsation of the liver
• Muller’s sign : pulsation of the uvula
• Wide pulse pressure ( > 40 mm Hg bet SBP & DBP
)
• Pulsus bisferious : 2 palpable pulses during systole
• Exam directed towards Marfan’s syndrome ,
rheumatoid spondylitis, syphilis, essential HPN and
VSD
PE OF CHRONIC AORTIC REGURGITATION (con’t)
• Outward and downward displacement of the apex beat
• Flow ( systolic ) murmur at the base : increased systolic
early peaking mid systolic crescendo- decrescendo
ejection murmur
• Decrescendo diastolic blow ( aortic backflow of blood ;
increases during sitting , expiration and leaning forward )
at the left sternal border : valvar cause of AR ; right
sternal border ( aortic root pathology as the cause of AR )

• “ Austin Flint “ murmur : mistaken for MS because of mid

or late diastolic rumble at the apical area due to
functional or relative inhibition of mitral valve opening by
the AR jet and sudden LV distention
 CONGENITAL HEART DISEASES

* Note for clubbing and cyanosis and its distribution

CONGENITAL HEART DISEASES

1. Cyanotic or Non-cyanotic
2. Clubbing or non clubbing
3. Orientation of the visceral structures
4. Dextrocardia or Levocardia
5. Cardiac Rhythm
 ASD
• ASD (ostium secundum defect) occurs as an isolated
anomaly in 5% to 10% of all congenital heart defects.
• more common in females than in males (male-female ratio
of 1:2).
• About 30% to 50% of children with congenital heart
defects have an ASD as part of the cardiac defect
• ASDs, is most commonly located at the entry of the
superior vena cava (SVC) into the RA
ASD
 ASD PATHOLOGY
• 1. Three types of ASDs exist—secundum defect, primum defect, and
sinus venosus defect. Patent foramen ovale (PFO) does not ordinarily
produce intracardiac shunts .
• 2. Ostium secundum defect is the most common type of ASD,
accounting for 50% to 70% of all ASDs. This defect is present at the
site of fossa ovalis, allowing left-to-right shunting of blood from the left
atrium (LA) to the right atrium (RA) . Anomalous pulmonary venous
return is present in about 10% of cases.
• 3. Ostium primum defects occur in about 30% of all ASDs, if those that
occur as part of a complete ECD are included . Isolated ostium
primum ASD occurs in about 15% of all ASDs.
 ASD PATHOLOGY
• 4. Sinus venosus defect, which occurs in about 10% of all ASDs, is
most commonly located at the entry of the superior vena cava (SVC)
into the RA (superior vena caval type) and rarely at the entry of the
inferior vena cava (IVC) into the RA (inferior vena caval type). The
right pulmonary veins may drain anomalously into the RA. More
commonly, the right pulmonary veins enter normally into the LA at the
point near the ASD and only appear to enter anomalously into the RA.
True anomalous venous return of the right pulmonary veins into the
IVC occurs in the scimitar syndrome
• 5. An unroofed coronary sinus is a rare communication between the
coronary sinus and the LA, which produces clinical pictures similar to
other types of ASD.
• 6. Mitral valve prolapse (MVP) occurs in 20% of patients with either
ostium secundum or sinus venosus defects.
 ASD
History:
• Infants and children with ASDs are usually asymptomatic.
Rarely, congestive heart failure (CHF) can develop in
infancy. If a large defect is untreated, CHF and pulmonary
hypertension develop in adults who are in their 20s and 30s.
With or without surgery, atrial arrhythmias (flutter or
fibrillation) may occur in adults.
• Infective endocarditis does not occur in patients with
isolated ASDs. Therefore, subacute bacterial endocarditis
(SBE) prophylaxis is unnecessary for these patients unless
their condition is associated with other defects.
Cerebrovascular accident, resulting from paradoxical
embolization through an ASD, is a rare complication
 ASD
• Physical Examination
– 1. A relatively slender body build is typical. (The
body weight of many is less than the 10th
percentile.)
– 2. A widely split and fixed S2 and a grade 2-3/6
systolic ejection murmur are characteristic findings
of ASD in older infants and children. With a large left-
to-right shunt, a mid-diastolic rumble resulting from
relative tricuspid stenosis may be audible at the
lower left sternal border.
– 3. The typical auscultatory findings may be absent in
infants, even infants who have a large defect.
 ASD
widely split and fixed S2 and a
grade 2-3/6 systolic ejection murmur
 VSD
• most common form of congenital heart
defect and accounts for 15% to 20% of all
such defects, not including those occurring
as part of cyanotic congenital heart
defects.
VSD
 VSD
History
• 1. With a small VSD, the patient is asymptomatic with
normal growth and development.
• 2. With a moderate to large VSD, delayed growth and
development, decreased exercise tolerance, repeated
pulmonary infections, and CHF are relatively common
during infancy.
• 3. With long-standing pulmonary hypertension, a
history of cyanosis and a decreased level of activity
may be present.
 VSD
• Physical Examination
1.Infants with small VSDs are well developed and acyanotic. Before 2 or 3
months of age, infants with large VSDs may have poor weight gain or show
signs of CHF. Cyanosis and clubbing may be present in patients with
pulmonary vascular obstructive disease (Eisenmenger's syndrome).
2.A systolic thrill may be present at the lower left sternal border. Precordial
bulge and hyperactivity are present with a large-shunt VSD.
3.The intensity of the P2 is normal with a small shunt and moderately
increased with a large shunt. The S2 is loud and single in patients with
pulmonary vascular obstructive disease. A grade 2-5/6 regurgitant systolic
murmur is audible at the lower left sternal border. It may be holosystolic or
early systolic. An apical diastolic rumble is present with a moderate to large
shunt.
4.With infundibular VSD, a grade 1-3/6 early diastolic decrescendo murmur of
AR may be audible. This murmur occurs because of herniation of an aortic
cusp.
 VSD

Cardiac findings of a small ventricular septal defect . A

regurgitant systolic murmur is best audible at the lower left
sternal border; it may be holosystolic or less than holosystolic.
Occasionally, the heart murmur is in early systole. A systolic thrill
(dots) may be palpable at the lower left sternal border. The S2
splits normally, and the P2 is of normal intensity.
 VSD

Cardiac findings of a large ventricular septal defect . A classic

holosystolic regurgitant murmur is audible at the lower left sternal border.
A systolic thrill is also palpable at the same area (dots). There is usually a
mid-diastolic rumble, resulting from relative mitral stenosis, at the apex.
The S2 is narrowly split, and the P2 is accentuated in intensity.
Occasionally an ejection click (EC) may be audible in the upper left
sternal border when associated with pulmonary hypertension. The heart
murmurs shown without solid borders are transmitted from other areas
and are not characteristic of the defect. Abnormal sounds are shown in
black. Insp., inspiration.
 Patent Ductus Arteriosus
• PDA occurs in 5% to 10% of all congenital heart defects,
excluding premature infants. It is more common in females than
in males (male-female ratio of 1:3). PDA is a common problem in
premature infants

• PATHOLOGY
– 1. There is a persistent patency of a normal fetal structure
between the left PA and the descending aorta, that is, about 5
to 10 mm distal to the origin of the left subclavian artery.
– 2. The ductus is usually cone shaped with a small orifice to
the PA, which is restrictive to blood flow. The ductus may be
short or long, straight or tortuous.
Patent Ductus Arteriosus
 PDA
• 1. Patients are usually asymptomatic when the
ductus is small.
• 2. A large-shunt PDA may cause a lower
respiratory tract infection, atelectasis, and CHF
(accompanied by tachypnea and poor weight
gain).
 PDA
Physical Examination
• 1. Tachycardia and exertional dyspnea may be
present in children with a large-shunt PDA. With
pulmonary vascular obstructive disease, a right-to-left
ductal shunt results in cyanosis only in the lower half
of the body (i.e., differential cyanosis).
• 2. The precordium is hyperactive. A systolic thrill may
be present at the upper left sternal border. Bounding
peripheral pulses with wide pulse pressure (with
elevated systolic pressure and lower diastolic
pressure) are characteristic findings.
 PDA
• 3. The P2 is usually normal, but its intensity may be accentuated
if pulmonary hypertension is present. A grade 1-4/6 continuous
(“machinery”) murmur is best audible at the left infraclavicular
area or upper left sternal border. The heart murmur may be
crescendo systolic at the upper left sternal border in small
infants or infants with pulmonary hypertension. An apical
diastolic rumble may be heard when the PDA shunt is large.
 TETRALOGY OF FALLOT
- occurs in 10% of all congenital heart defects. This is the
most common cyanotic heart defect seen in children
beyond infancy.
PATHOLOGY :
- 1. The original description of TOF included the following four
abnormalities: a large VSD, right ventricular outflow tract
obstruction, RVH, and overriding of the aorta. In actuality,
only two abnormalities are required—a VSD large enough
to equalize pressures in both ventricles, and a right
ventricular outflow tract obstruction. The RVH is secondary
to the right ventricular outflow tract obstruction and the
VSD. The overriding of the aorta
 TETRALOGY OF FALLOT
PATHOLOGY : ( con’t. )
- 2. The VSD in TOF is a perimembranous defect with
extension into the subpulmonary region.
- 3. The right ventricular outflow tract obstruction is most
frequently in the form of infundibular stenosis (45%). The
obstruction is rarely at the pulmonary valve level(10%). A
combination of the two may also occur (30%). The
pulmonary valve is atretic in the most severe form of the
anomaly (15%). In some children, pulmonary atresia
develops with time
 TETRALOGY OF FALLOT
- 4. The pulmonary annulus and main PA are hypoplastic in
most patients. The PA branches are usually small, with
variable peripheral stenosis. Obstruction at the origin of the
left PA is particularly common. Systemic collateral arteries
feeding into the lungs are occasionally present, especially
in severe cases of TOF.
- 5. Right aortic arch is present in 25% of cases. 6. In about
5% of TOF patients, abnormal coronary arteries are
present. The most common abnormality is the anterior
descending branch arising from the right coronary artery
and passing over the right ventricular outflow tract, which
prohibits a surgical incision in the region.
TETRALOGY OF FALLOT
 TETRALOGY OF FALLOT
HISTORY
1. A heart murmur is audible at birth.
2. Most patients are symptomatic with cyanosis at
birth or shortly thereafter. Dyspnea on exertion,
squatting, or hypoxic spells develop later, even in
mildly cyanotic infants.
3. Infants with acyanotic TOF may be asymptomatic
or may show signs of CHF from a large left-to-right
ventricular shunt.
4. Immediately after birth, severe cyanosis is seen in
patients with TOF and pulmonary atresia.
 TETRALOGY OF FALLOT
HISTORY
1.Infants with acyanotic TOF gradually become cyanotic. Patients who
are already cyanotic become more cyanotic as a result of the
worsening condition of the infundibular stenosis and polycythemia.
2.Polycythemia develops secondary to cyanosis.*
3.Physicians need to watch for the development of relative iron-
deficiency (i.e., hypochromic) state. *
4.Hypoxic spells may develop in infants
5.Growth retardation may be present if cyanosis is severe. *
6.Brain abscess and cerebrovascular accident rarely occur .*
7.Subacute bacterial endocarditis (SBE) is occasionally a complication.*
8.Some patients, particularly those with severe TOF, develop AR.
9.Coagulopathy is a late complication of a long-standing cyanosis. *

* This occurs in all types of cyanotic congenital heart defects.

 TETRALOGY OF FALLOT
PHYSICAL EXAMINATION
1. Varying degrees of cyanosis, tachypnea, and clubbing are present. ( Cyanotic
vs. non cyanotic )
2. An RV tap along the left sternal border and a systolic thrill at the upper and
mid-left sternal borders are commonly present (50%).
3. An ejection click that originates in the aorta may be audible. The S2 is usually
single, because only the aortic component can be heard. A long, loud (grade3-
5/6) ejection-type systolic murmur is heard at the mid and upper left sternal
borders. This murmur originates from the PS but may be easily confused with
the holosystolic regurgitant murmur of a VSD. The more severe the obstruction
of the right ventricular outflow tract, the shorter and softer the systolic murmur.
In a deeply cyanotic neonate with TOF with pulmonary atresia, heart murmur is
either absent or very soft, although a continuous murmur representing PDA
may occasionally be audible.
4. In the acyanotic form, a long systolic murmur, resulting from VSD and
infundibular stenosis, is audible along the entire left sternal border, and
cyanosis is absent. Thus auscultatory findings resemble those of a small-shunt
VSD
 TETRALOGY OF FALLOT

A long ejection systolic murmur at the upper and mid left sternal
border and a loud, single S2 are characteristic auscultatory findings
of TOF. EC, ejection click.
HPN
 HYPERTENSION
• Most : no specific symptoms
• Although popularly considered a symptom of elevated
arterial pressure, headache generally occurs only in
patients with severe hypertension.
• Characteristically, a "hypertensive headache" occurs in
the morning and is localized to the occipital region.
• Other nonspecific symptoms that may be related to
elevated blood pressure include dizziness, palpitations,
easy fatigability, and impotence.
 PE OF HYPERTENSION
• Body habitus, including weight , height and heart rate
• blood pressure should be measured in both arms, and
preferably in the supine, sitting, and standing positions to
evaluate for postural hypotension
• enlarged thyroid gland ? s/s of hypo- or hyperthyroidism
• funduscopic examination (arteriolar light reflex,
arteriovenous crossing defects, hemorrhages and
exudates, and, in patients with malignant hypertension,
papilledema.), auscultation for bruits over the carotid and
femoral arteries, and palpation of femoral and pedal
pulses.
 PE OF HYPERTENSION
• loud second heart sound due to closure of the aortic valve
and an S4 gallop, attributed to atrial contraction against a
noncompliant left ventricle.
• Left ventricular hypertrophy may be detected by an
enlarged, sustained, and laterally displaced apical impulse.
• Abdominal bruit, particularly a bruit that lateralizes and
extends throughout systole into diastole, raises the
possibility of renovascular hypertension. Kidneys of patients
with polycystic kidney disease may be palpable in the
abdomen. The physical examination should also include
evaluation for signs of CHF and a neurologic examination.
to to

to to
 CORONARY ARTERY DISEASE
• imbalance between myocardial oxygen supply
and demand.
• most common cause of myocardial ischemia :
atherosclerotic disease of an epicardial coronary
artery (or arteries) sufficient to cause a regional
reduction in myocardial blood flow and
inadequate perfusion of the myocardium supplied
by the involved coronary artery
 CORONARY ARTERY DISEASE

• typical patient with angina is a man older

than 50 years or a woman older than 60
years of age who complains of chest
discomfort, usually described as
heaviness, pressure, squeezing,
smothering, or choking, and only rarely as
frank pain.
 CORONARY ARTERY DISEASE

• Patients place their hand over the sternum, sometimes with a

clenched fist, to indicate a squeezing, central, substernal
discomfort (Levine's sign).
• crescendo-decrescendo in nature, typically lasts 2 to 5 min, and
can radiate to either shoulder and to both arms (especially the
ulnar surfaces of the forearm and hand). It can also arise in or
radiate to the back, interscapular region, root of the neck, jaw,
teeth, and epigastrium.
• Angina is rarely localized below the umbilicus or above the
mandible.
• A useful finding in assessing the patient with chest discomfort 
does not radiate to the trapezius muscles; such a radiation
pattern is more typical of pericarditis.
 CORONARY ARTERY DISEASE

• typically caused by exertion (e.g., exercise, hurrying, or sexual

activity) or emotion (e.g., stress, anger, fright, or frustration) and are
relieved by rest, they may also occur at rest and while the patient is
recumbent (angina decubitus).
• may be awakened at night by typical chest discomfort and dyspnea.
Nocturnal angina may be due to episodic tachycardia, diminished
oxygenation as the respiratory pattern changes during sleep, or
expansion of the intrathoracic blood volume that occurs with
recumbency; the latter causes an increase in cardiac size (end-
diastolic volume), in wall tension, and in myocardial oxygen demand
that lead to ischemia and transient LV failure.
• examined for peripheral arterial disease (intermittent claudication,),
stroke, or transient ischemic attacks
 CORONARY ARTERY DISEASE

PE :
• may reveal evidence of atherosclerotic disease at other sites, such as
an abdominal aortic aneurysm, carotid arterial bruits, and diminished
arterial pulse in the lower extremities, or of risk factors for
atherosclerosis, such as xanthelasmas and xanthomas
• Fundoscopy : may reveal an increased light reflex and arteriovenous
nicking as evidence of hypertension
• signs of anemia, thyroid disease, and nicotine stains on the fingertips
from cigarette smoking.
• Palpation may reveal cardiac enlargement and abnormal contraction
of the cardiac impulse (left ventricular akinesia or dyskinesia).
 CORONARY ARTERY DISEASE

PE :
• arterial bruits, a third and/or fourth heart sound, and, if acute ischemia or
previous infarction has impaired papillary muscle function, an apical systolic
murmur due to mitral regurgitation ( especially on a left lateral decubitus
position. )
• can cause transient LV failure with the appearance of a third and/or fourth
heart sound, a dyskinetic cardiac apex, mitral regurgitation, and even
pulmonary edema.
• Ischemic unlikely if :
– if there is tenderness of the chest wall, localization of the discomfort with a
single fingertip on the chest, or reproduction of the pain with palpation of
the chest
– During inspiration and cough ( pleuritic type of chest pain )
– Accompanied with heartburn manifestations ( burping, flatulence ,
bloatedness )
Modified from L Goldman et al: Circulation 64:1227, 1981
 COR PULMONALE
• right ventricular (RV) enlargement
secondary to any underlying cardiac or
pulmonary disease.
• Pulmonary hypertension is the most
common cause  RV failure
• exertional dyspnea, fatigue, angina pectoris
that may represent RV ischemia, syncope,
near syncope, and peripheral edema.
 COR PULMONALE
• Increased jugular venous pressure, a
reduced carotid pulse, and a palpable RV
impulse. Most patients have an increased
pulmonic component of the second heart
sound, a right-sided fourth heart sound,
and tricuspid regurgitation.
• Peripheral cyanosis and/or edema tend to
occur in later stages of the disease.
CAUSES OF COR PULMONALE
 PERICARDIUM
• double-layered sac; the visceral
pericardium is a serous membrane that is
separated by a small quantity (15 to 50
mL) of fluid, an ultrafiltrate of plasma, from
the fibrous parietal pericardium.
 PERICARDITIS

• Chest pain usually in infectious types,

hypersensitivity or autoimmunity
• Chest pain often absent in slowly
developing tuberculous, postirradiation,
neoplastic, or uremic pericarditis.
• often severe, retrosternal and left
precordial, and referred to the neck, arms,
or the left shoulder.
 PERICARDITIS

• Often the pain is pleuritic, consequent to

accompanying pleural inflammation, i.e., sharp
and aggravated by inspiration, coughing, and
changes in body position, but sometimes it is a
steady, constricting pain that radiates into either
arm or both arms and resembles that of
myocardial ischemia; therefore, confusion with
acute myocardial infarction (AMI) is common.
 PERICARDITIS

• pericardial pain may be relieved by sitting

up and leaning forward and is intensified
by lying supine.
• Narrow pulse pressure
 PERICARDITIS

• pericardial friction rub, audible in about 85% of patients,

may have up to three components per cardiac cycle, is
high-pitched, and is described as rasping, scratching, or
grating
• described as triphasic, with systolic and early (passive
ventricular filling) and late (atrial systole) diastolic
components, more commonly a biphasic (systole and
diastole) or a monophasic rub may be heard.
 PERICARDITIS

• it can be elicited sometimes only when the diaphragm of

the stethoscope is applied firmly to the chest wall at the
left lower sternal border. It is heard most frequently at
end-expiration with the patient upright and leaning
forward. The rub is often inconstant, and the loud to-and-
fro leathery sound may disappear within a few hours,
possibly to reappear on the following day. A pericardial rub
is heard throughout the respiratory cycle, while a pleural
rub disappears when respiration is suspended.
 TAMPONADE
• accumulation of fluid in the pericardial space in a quantity
sufficient to cause serious obstruction to the inflow of blood
to the ventricles
• three most common causes of tamponade are neoplastic
disease, idiopathic pericarditis, and pericardial effusion
secondary to renal failure.
• bleeding into the pericardial space either following cardiac
operations and trauma (including cardiac perforation during
cardiac catheterization, percutaneous coronary intervention,
or insertion of pacemaker wires) or from tuberculosis and
hemopericardium. The latter may occur when a patient with
any form of acute pericarditis is treated with anticoagulants.
 TAMPONADE
• Three principal features of tamponade (Beck's triad) are
hypotension, soft or absent heart sounds, and jugular
venous distention with a prominent x descent but an absent
y descent.
• critical state may be as small as 200 mL when the fluid
develops rapidly or >2000 mL in slowly developing effusions
when the pericardium has had the opportunity to stretch
and adapt to an increasing volume.
• volume of fluid required to produce tamponade also varies
directly with the thickness of the ventricular myocardium
and inversely with the thickness of the parietal pericardium.
 PARADOXICAL PULSE
• In significant pericardial effusion with tamponade but also
seen in RV infarction , constrictive pericarditis,
hypovolemic shock, acute and chronic obstructive airways
disease, and pulmonary embolus.
• greater than normal ( 10 mmHg ) inspiratory decline in
systolic arterial pressure ;
• detected by palpating weakness or disappearance of the
arterial pulse during inspiration, but usually
sphygmomanometric measurement of systolic pressure
during slow respiration is required
Thank you for your
kind attention !