Cardiovascular system

1. CARDIOVASCULAR SYSTEM
(HARRISON’S)
MOTE SRIKANTH
CV disease is now
the most common
cause of death
worldwide

2. WHAT ARE THE CARDIAC SYMPTOMS ??
 Chest pain
 Palpitations
 Dyspnea
 Dizziness & Syncope
 Easy fatigability
 Oliguria
 Swelling of feet
 Loss of appetite & weight (due to congestive
hepatopathy & gastropathy)
 Ascites
 Jaundice (due to cardiac cirrhosis)
 Recurrent respiratory tract infections (due to pulmonary
congestion)

3. WHAT DO THEY INDICATE ??
SYMPTOM CAUSE/ INDICATES
1) CHEST DISCOMFORT Myocardial ischemia caused by
an imbalance between the
heart’s oxygen supply and
demand
2) EASY FATIGABILITY
PERIPHERAL EDEMA
DYSPNEA (due to pulm. edema)
Reduction of the pumping
ability of heart
3) EDEMA (+ all other symptoms
resembling those of myocardial
failure)
Obstruction to blood flow (eg:
vascular stenosis)
4) PALPITATIONS
SYNCOPE
DYSPNEA
HYPOTENSION
Abnormal cardiac rate or
rhythm (Cardiac arrhythmias)

4. ARE THESE SYMPTOMS RESTRICTED TO ONLY
CVS ??
SYMPTOM OTHER POSSIBLE CAUSES
DYSPNEA • Pulmonary disease
• Marked obesity
• Anxiety, etc.
CHEST DISCOMFORT • Other cardiac causes (apart
from myocardial ischemia)
• Non-cardiac causes
EDEMA • Primary renal disease
• Hepatic cirrhosis
SYNCOPE • Neurological conditions
NOPE !!

5. HOW WILL YOU KNOW IF HEART DISEASE IS
RESPONSIBLE FOR THESE SYMPTOMS ??
 By carrying out a careful clinical examination
 Supplemented by non-invasive testing (eg:
electrocardiography at rest & during exercise,
echocardiography) & other forms of myocardial
imaging
Myocardial or coronary function
that may be adequate at rest
but insufficient during exertion
 dyspnea, chest discomfort
(during activity) are
characteristic of patients with
heart disease

6. SO NOW ROUGHLY YOU HAVE COME TO KNOW THAT
IT IS CARDIAC PATHOLOGY..THEN WHAT NEXT ??
To come to a complete cardiac diagnosis, following
considerations to be made:
ELEMENTS QUESTIONS
1. UNDERLYING
ETIOLOGY
• Congenital ?
• Hypertensive ?
• Ischemic ?
• Inflammatory in origin ?
2. ANATOMIC
ABNORMALITIES
• Chambers involved?
• Are they hypertrophied?
dilated? both?
• Valves affected?
• Regurgitant? Stenotic?
• Pericardial involvement?
3. PHYSIOLOGIC
DISTURBANCES
• Arrhythmia present?
• Evidence of M.ischemia or
CHF
4. FUNCTIONAL
DISABILITY
• How strenuous is the
physical activity required to
elicit symptoms?
(NYHA classification)

7. 4A:

8. 4B: (GRADING OF DYSPNEA)
Grade 1: Dyspnea occurring during unaccustomed
exertion (classical eg: running up 2 long flights of
stairs)
Grade 2: during accustomed exertion (classical eg:
climbing up 2 long flights of stairs)
Grade 3: during minimal exertion (classical eg:
walking from room to room)
Grade 4: at rest

9. FOR EXAMPLE,
 In a patient who presents with exertional chest
discomfort, the identification of myocardial ischemia as
the etiology is of great clinical importance. However the
simple recognition of ischemia is insufficient to formulate
a therapeutic strategy or prognosis until the underlying
anatomic abnormalities responsible for the myocardial
ischemia [eg: coronary atherosclerosis or aortic
stenosis] are identified and a judgment is made about
whether other physiologic disturbances that cause an
imbalance between myocardial oxygen supply and
demand [eg: severe anemia, thyrotoxicosis] play
contributory roles. Finally the severity of the disability
should govern the extent and tempo of the workup and
strongly influence the therapeutic strategy that is
selected

10. The establishment of a
correct and complete cardiac
diagnosis usually
commences with
i. History
ii. Physical examination
iii. 5 types of lab tests
5 LABORATORY TESTS
• ECG
• Non-invasive imaging examinations (echocardiogram, CT
imaging, MRI, etc.)
• Blood tests to assess risk (eg: lipid determinations, CRP) or
cardiac function (eg: BNP)
• Occasionally specialized invasive examinations (cardiac
catheterization, coronary arteriography)
• Genetic tests to identify monogenic cardiac diseases (eg:
hypertrophic cardiomyopathy, Marfan’s syndrome, sudden
death assoc. with a prolonged QT interval syndrome)
In history taking of a patient
with known or suspected CV
disease, particular attention
should be directed to family
history
WHY ??
Coz familial clustering is
common in many forms of
heart disease:
• hypertrophic
cardiomyopathy
• Marfan’s syndrome
• sudden death assoc. with a
prolonged QT interval
syndrome

11. CAN YOU PREVENT CAD ?? HOW ??
Prevention begins with
 Risk assessment
 Lifestyle changes (eg: achieving optimal weight,
physical activity, smoking cessation, etc.)
 Aggressive treatment of all abnormal risk factors
(HT, hyperlipidemia, DM)
YES !!

12. MANAGEMENT:
In absence of
evidence of
heart disease
In absence of
evidence of
heart disease
but the patient
has one or
more risk
factors
Asymptomatic /
mildly
symptomatic
patients with
valvular heart
disease (that is
anatomically
severe)
In patients
with CAD
Inform the pt.
clearly of this
assessment and
NOT BE asked
to return at
intervals
for repeated
examination
Develop a plan for
their reduction & pt.
should be retested
at intervals to
assess the efficacy
in risk
reduction
Evaluated
periodically every
6-12 months by
clinical & non-
invasive
examinations
Rx: medical,
percutaneous
coronary
intervention,
surgical
revascularization

13. Why scenario 3 type of patient needs to be evaluated
every 6-12 months ??
Coz in case of early signs of deterioration of ventricular
function signifies the need for surgical treatment before the
development of disabling symptoms, irreversible
myocardial damage, etc.
Can we do revascularization for all scenario 4 patients??
The mere presence of angina pectoris &/ demonstration of
critical coronary artery narrowing at angiography should
not reflexively evoke a decision to treat patient by
revascularization.
Instead it must be limited to patients with CAD whose
angina has not responded adequately to medical
treatment or in whom revascularization has been shown to
improve the natural history (eg: acute coronary syndrome
or multivessel CAD with left ventricular dysfunction)

14. SOMETHING ABOUT HEART MURMUR: (EXTRA)
 Majority of heart murmurs are midsystolic and soft
(grades 1-2)
Do all murmurs require
echocardiography ??
NOPE !!

15. EVALUATION OF HEART MURMUR: (PG 1441)

16. NOW LET US GO IN DETAIL WITH EXAMINATION
PART..
2 parts
GENERAL
PHYSICAL
EXAMINATION
CARDIOVASCULAR
EXAMINATION

17. GENERAL PHYSICAL EXAMINATION:
1. General appearance of patient
- built & nourishment
- posture
- dyspneic ?
- diaphoretic ?
- in pain / resting quietly ?
- does the patient choose to avoid certain body
positions to reduce/ eliminate pain ?
- mental status
- level of alertness
- mood

18. 2. SKIN
CONDITION INDICATES
1) CENTRAL CYANOSIS Significant right-to-left shunting at the
level of heart / lungs
2) PERIPHERAL CYANOSIS Reduced blood flow to extremity due
to small vessel constriction (as in
severe heart failure/ shock/ peripheral
vascular disease)
3) DIFFERENTIAL CYANOSIS • Large PDA
• Secondary pulmonary HT with right-
to-left shunting at great vessel level
4) TELANGIECTASIAS (on face) • Advance mitral stenosis
• Scleroderma
5) TAN/ BRONZE DISCOLORATION
OF SKIN
Hemochromatosis is the cause of
assoc. heart failure
6) JAUNDICE • Advanced right heart failure
• Congestive hepatomegaly (cardiac
cirrhosis)

19. 7) CUTANEOUS ECCHYMOSES Patient is taking Vit K antagonists or
antiplatelet agents (eg: aspirin)
8) XANTHOMAS Lipid disorders

20. 3. HEAD & NECK:
 Dentition & oral hygiene
 Ocular examination
 Face
FEATURE CONDITION
1) High-arched palate Marfan’s syndrome & other
connective tissue disease
syndromes
2) Bifid uvula Loeys-Dietz syndrome
3) Orange tonsils Tangier disease
FEATURE CONDITION
1) Blue sclera Osteogenesis imperfecta
Many patients with
congenital heart disease
have associated
hypertelorism + low-set
ears + micrognathia
FEATURE CONDITION
1) INFLAMMED PINNA /
SADDLE NOSE
DEFORMITY
Relapsing polychondritis

21. 4. CHEST:
FEATURES INDICATES
1) Scars ?
2) Prominent venous
collateral pattern
Subclavian / vena caval
obstruction
3) Thoracic cage
abnormalities
• Pectus carinatum
(pigeon chest)
• Pectus excavatum
(funnel chest)
• Barrel chest
Connective tissue disease
syndromes
Obstructive Lung disease
4) Severe kyphosis Auscultate for murmur of
AR
5) Straight back syndrome Mitral valve prolapse
6) Asymmetric chest wall
with anterior displacement
of left hemithorax
Cyanotic congenital heart
disease

22. 5. ABDOMEN
FEATURE INDICATES
1) Point of maximum
cardiac impulse in
epigastrium
Advanced obstructive lung
disease
2) Enlarged & tender liver Chronic heart failure
3) Systolic pulsations over
liver
Tricuspid regurgitation
4) Splenomegaly Infective endocarditis
5) Ascites • Chronic right heart failure
• Constrictive pericarditis
• Hepatic cirrhosis
• Intraperitoneal
malignancy
6) Arterial bruit over
abdomen
High grade atherosclerotic
disease

23. 6. EXTREMITIES:
FEATURE INDICATES
1) Temperature ?
2) Color ?
3) Clubbing Central right-to-left shunting
4) Fingerized thumb Holt-Oram syndrome
5) - Arachnodactyly
- Positive “wrist” sign
(overlapping of thumb
& 5th finger around
the wrist) /
- Positive “thumb” sign
(protrusion of the
thumb beyond the ulnar
aspect of hand when the
fingers are clenched over
the thumb in a fist)
Marfan’s syndrome

24. 6) - Janeway lesions (non tender,
slightly raised hemorrhages on palms &
soles)
- Osler’s nodes (tender, raised
nodules on the pads of the fingers or
toes)
- Splinter hemorrhages
Endocarditis
7) Lower extremity or pre-sacral edema
(+increased JVP)
(-increased JVP)
(-increased JVP
+ varicosities/ venous ulcers –medial/
brownish cutaneous discoloration from
hemosiderin discoloration –
EBURNATION)
• Chronic heart failure
• Constrictive pericarditis
• Lymphatic/venous obstruction
• Venous insufficiency (MC)
8) Muscular atrophy / absence of hair
along an extremity
• Severe arterial insufficiency
• Primary neuromuscular
disorder

25. CARDIOVASCULAR EXAMINATION:
1. Jugular venous pressure & waveform
2. BP
3. Arterial pulse
4. Inspection & palpation of heart
5. Cardiac auscultation

26. 1) JVP:
 AIM: to estimate the volume status
Which vein is used to measure JVP?
Internal jugular vein is preferred. External Jugular
vein is less reliable coz of:
i. Does not directly drain into SVC & Rt. atrium
ii. Has valves
How do you measure JVP ?
Traditionally has been measured as vertical distance
between the top of the jugular venous pulsation &
Angle of Louis.
A distance > 4.5cm at 30 degree elevation is
considered abnormal
Finding of an
elevated JVP
implies a
cardiovascular
pathology

27. Why clavicle is preferred over Angle of Louis as a
reference point?
 Coz the actual distance between the mid-right
atrium and the angle of Louis varies considerably
as a function of both body size & the patient angle
at which assessment is made (30/45/60 degree)
 Venous pulsations above clavicle in the sitting
position (with the legs dangling below the bedside)
are clearly abnormal as the distance between the
clavicle & the right atrium is at least 10 cm

28. Differentiation btw venous & arterial pulsation ?
VENOUS PULSATION ARTERIAL PULSATION
1) Lateral to SCM Medial to SCM
2) Waves disappear when
pressure given at root of neck
Not easily obliterated with
palpation
3) Usually biphasic Monophasic
4) Easily seen than felt Easily felt than seen
5) Change with changes in
posture or inspiration

29. Waves ??
‘ WAVES MECHANISM
‘a' wave [MOST
DOMINANT WAVE] +
Right atrial contraction
‘c’ wave + Closure & bulging of
tricuspid valve
‘x’ descent - Atrial relaxation with
downward descent of
tricuspid valve
‘v’ wave + Passive right atrial filling
during ventricular systole
‘y’ descent - Right ventricular filling with
atrial emptying

30. Prominent ‘a’ wave??
 Tricuspid stenosis/atresia
 Mitral stenosis
 Pulmonary stenosis
 Pulmonary HT
‘a’ wave absent in??
 Atrial fibrillation
Cannon ‘a’ wave??
Very large ‘a’ wave is known as cannon wave. Seen
in
 AV dissociation
 Right atrial contraction against a closed tricuspid
valve

31. Kussmaul’s sign/ Venous pulsus paradoxus ?
 In normally healthy persons, the venous pressure
should fall by at least 3 mmHg with inspiration (due
to sucking of blood into right atrium)
 Kussmaul’s sign – Either a rise or a lack of fall of
JVP with inspiration
 Classically associated with constrictive pericarditis
 Also seen in patients with
- restrictive cardiomyopathy
- massive pulmonary embolism
- right ventricular infarction
- advanced left ventricular systolic heart failure

32. Other methods of eliciting venous HT?
 Abdomino-jugular reflex
 Passive leg elevation
Abdomino-jugular reflex?
 Elicited with firm & consistent pressure over the
upper portion of the abdomen, preferably over the
right upper quadrant, for at least 10 sec.
 + : Sustained rise of > 3 cm in JVP for at least 15
sec after release of the hand (as hepatic venous
reservoir gets compressed)
 Useful in predicting pulmonary artery wedge
pressure in excess of 15 mmHg in patients with
heart failure

33. 2) BP:
How to measure BP?
 Best measured in seated position with the arm at
the level of the heart, using an appropriately sized
cuff, after 5-10 mins of relaxation
 When measured in supine position, arm must be
raised to bring it to the level of mid-right atrium
 Cuff should be inflated to 30 mmHg above the
expected systolic pressure and the pressure
released at a rate of 2-3 mmHg /sec
Systolic & diastolic pressures are defined by?
1st & 5th Korotkoff sounds respectively

34. BP measured at?
Best assessed at brachial artery level (though it can
be measured at radial, popliteal or pedal pulse level)
BP should be measured in both arms and the
difference should be less than 10 mmHg.
>10 mmHg indicates ?
 Atherosclerotic/
 Inflammatory subclavian artery disease
 Supravalvular aortic stenosis (right sided higher
BP)
 Pre-ductal coarctation of aorta (right sided higher
BP)
 Unilateral occlusive disease of arteries

35. Systolic leg pressures are usually as much as 20
mmHg higher than systolic arm pressures. Greater
leg-arm pressure differences are seen in?
 Chronic severe AR
 Extensive & calcified lower extremity peripheral
arterial disease
White coat HT?
 Defined by
 at least 3 separate clinic-based measurements >140/90
mmHg &
 at least 2 non-clinic based measurements <140/90
mmHg
 in the absence of any evidence of target organ damage
 May not benefit from drug therapy

36. Masked HT?
Suspected when normal or even low BPs are
recorded in patients with advanced atherosclerotic
disease, especially when evidence of target organ
damage is present or bruits are audible.
Orthostatic hypotension?
 Fall in systolic pressure > 20 mmHg or in diastolic
pressure > 10 mmHg in response to assumption of
the upright posture from a supine posture within 3
mins
 Common cause of postural lightheadedness/
syncope
 CAUSES: advanced age, DM, hypovolaemia (blood
or fluid loss), certain medications (centrally acting
anti HT)

37. 3) ARTERIAL PULSE:
Can aortic pulse be felt?
Yes. Best appreciated in the epigastrium just above the
level of umbilicus
Peripheral arterial pulses to be assessed?
 Subclavian
 Brachial
 Radial
 Ulnar
 Femoral
 Popliteal
 Dorsalis pedis
 Posterior tibial

38. Pulses to be examined for?
 Symmetry
 Volume
 Timing
 Contour
 Amplitude
 Duration
Radio-femoral delay?
 HT
 Suspected aortic coarctation
Character of pulse is best appreciated at?
Carotid level

39. PULSE SEEN IN
1) PULSUS PARVUS ET TARDUS (Parvus – low
in volume & amplitude; Tardus – slow rising pulse
with a late systolic peak)
AS
2) CORRIGAN’S / WATER-HAMMER Pul.
High volume pulse, sharp rise, ill sustained &
sharp fall
AR
3) ANACROTIC PULSE
Slow rising pulse (notched, or interrupted
upstroke ) with 2 systolic peaks
AS (some)
4) PULSUS BISFERIENS
Rapid rising pulse with 2 systolic peaks
• AS + AR
• Hypertrophic obstructive
cardiomyopathy (HOCM)
5) PULSUS ALTERNANS
Alternating small & large volume pulse in regular
rhythm
Severe LV systolic dysfunction
6) Fall in systolic pressure > 10 mmHg with
inspiration (PULSUS PARADOXUS)
• CARDIAC: Pericardial effusion,
Constrictive pericarditis,
Restrictive cardiomyopathies
• RS: Acute severe asthma, COPD
• SVC obstruction
Why normally fall
occurs ? – PJM 41

40. Causes of arterial bruit?
 Vascular obstruction
 AV fistula with enhanced flow
Auscultation of
carotid, subclavian,
abdominal aortic and
femoral artery bruits
should be routine

41. 4) INSPECTION OF HEART:
Apex beat?
Visible in left 5th ICS, ½ inch medial to mid clavicular line in
thin-chested adults
Abnormal visible pulsations?
Anywhere other than this expected location
Visible right upper parasternal pulsation is suggestive of?
Ascending aortic aneurysm disease
In thin, tall patients and patients with advanced obstructive
lung disease and flattened diaphragms; the cardiac
impulse may be visible in the epigastrium and should be
distinguished from a pulsatile liver edge

42. PALPATION OF HEART:
 Begins with the patient in the supine position at 30
degree and can be enhanced by placing the patient
in the left lateral decubitus position
Normal LV impulse?
 < 2cm in diameter
 Moves quickly away from the fingers
 Better appreciated at end expiration
 With the heart closer to ant. chest wall
Characteristics such as size, amplitude & rate of force
development should be noted

43. Right ventricular pressure or volume overload 
sternal lift
APEX BEAT INDICATES
1) Leftward & downward
displacement of an
enlarged apex beat
Enlargement of LV cavity
2) Sustained apex beat Pressure overload
• AS
• Chronic HT

44. 5) CARDIAC AUSCULTATION:
S1 indicates?
Mitral & tricuspid valve closure
S2 indicates?
Aortic & pulmonary valve closure
Ventricular systole?
Interval between S1 & S2
S2 consists of?
A2 + P2
A loud single or palpable P2 is suggestive of?
Pulmonary arterial HT

45. When is P2 considered to be loud?
 When its intensity exceeds that of A2 at the base/
 When it can be palpated in the area of proximal
main pulmonary artery (2nd left ICS)/
 When both components of S2 can be appreciated
at lower left sternal border or apex
Intensity of A2 decreases with?
Aortic stenosis
Intensity of P2 decreases with?
Pulmonary stenosis

46. CARDIAC MURMURS:
 Result from audible vibrations that are caused by
increased turbulence
 Intensity of a heart murmur is graded on a scale of
1-6
 Thrill is present with murmurs of >/= grade 4
Types of systolic murmurs based on timing?
 Early
 Mid – begins after S1 & ends before S2
 Late
 Holosystolic

47. MURMUR CONDITION
1) Early systolic murmur MR
2) Early systolic murmur
(increases in intensity with
inspiration) heard at left lower
sternal border
TR
3) Midsystolic murmur • AS (most common)
• Pulmonary valve stenosis
• HOCM
• Left-to-right shunting
• Several states associated with
accelerated blood flow in the
absence of structural heart
disease
- fever
- thyrotoxicosis
- pregnancy
- anemia
4) Late systolic murmur (heard
best at apex)
MVP
5) Holosystolic VSD

48. MURMUR OF BEST HEARD
1) AS 2nd right ICS with radiation into
carotids
2) HOCM Between lower left sternal border
& apex
3) PS 2nd left ICS
4) MR Over cardiac apex
5) VSD Mid-left sternal border (+thrill)
6) TR Lower left sternal border
(increases in intensity with
inspiration – Carvallo’s sign)

49. Diastolic heart murmurs always signify?
Structural heart disease
Classic cause of mid- to late diastolic murmurs?
MS
Classic example of continuous murmur?
That assoc. with PDA
2 types of benign continuous murmurs?
 Cervical venous hum – heard in children or
adolescents in supraclavicular fossa
 Mammary souffle of pregnancy – due to enhanced
arterial blood flow through engorged breasts

50. How can diagnostic accuracy be enhanced?
 Right sided events increase (except for pulmonic
ejection sound) in intensity with inspiration &
decrease with expiration
 Left sided events behave oppositely

51. THANK YOU