CARDIOVASCULAR SYSTEM EXAMINATION

Position & Exposure - with cardiac bed or supine

- bare chest
Exam: sequences - General exam:
- CVS exam: - (1) Pulse (2) BP (3) JVP (4) Precordium (5) Signs of HF

GENERAL EXAMINATION

Gen: Observation – Age, Sex, Conscious level, Comfortable position, Dyspnoeic/Not, Body
build Febrile / Not
Face - Malar flush
Eye - Anaemia, Jaundice, Subconjunctiva Haemorrhage, Corneal arcus, Xanthelesma
Nose - Ala nasi working
Mouth - Central cyanosis, Teeth & Gum healthy or not, Tonsilar enlargement
Neck - Goiter, Accessory muscles of respiration working or not, Visible pulsation
Hands - Clubbing, Splinter haemorrhage, Osler’s node, Janeway’s lesion, Petechiae
Peripheral cyanosis, Tar staining
Legs - Clubbing, Pitting oedema
 Splinter hemorrhages are tiny
blood spots that appear underneath
the nail. They look like splinters
and occur when tiny blood vessels
(capillaries) along the nail bed are
damaged and burst. The nail bed is
the skin underneath the nail.

Janeway lesions are

rare,non-tender, small
erythematous or
haemorrhagic macular,
papular or nodular lesions
on the palms or soles only a
few millimeters in diameter
that are associated with
infective endocarditis

Osler's nodes are

painful, red, raised
lesions found on
the hands and feet.
They are
associated with a
number of
conditions,
including infective
endocarditis, and
are caused by
immune complex
deposition.
CVS EXAMINATION
I. Arterial Pulses – Radial pulse, (Brachial, Carotid, Femoral, Dorsalis Pedis)

(1) Rate (4) Character (7) Radio-femoral delay

(2) Rhythm (5) Condition of vessel wall (8) Other peripheral pulses
(3) Volume (6) Equality on both sides

Rate - Normal - 60-100/min (Count over 15 sec and multiply by 4)

- Abnormal - < 60/min - Bradycardia
> 100/min - Tachycardia
Rhythm - Normal - Regular
- Abnormal - Irregular rhythm - Regularly irregular
 - Irregularly irregular *AF → Pulsus deficit (HR>PR)
Volume - Normal - Moderate volume
- Abnormal - Low volume
High volume *AR → Collapsing pulse
Jerky (HOCM)
Character - Normal - No special character
- Abnormal - 1 better detection in carotid (*Never assess both side
simultaneously)
(1) Collapsing pulse (+ Corrigan’s sign1)
(2) Slow rising pulse / Plateau pulse1
(3) Pulsus bisferiens1
(4) Pulsus alternans1
(5) Pulsus paradoxus
(6) Pulsus bigeminus1
(7) Pulsus deficit
Condition of v/s wall - Normal - Not / just palpable
- Abnormal - Palpable - Severe atherosclerosis
Equality on both sides - Normal – Symmetry/Equal on both sides
- Abnormal – Asymmetry – Causes of unequal pulses ……
Radio-femoral delay - Normal - No radio-femoral delay
- Abnormal – Delay (+) – Causes of R-F delay ……
Other peripheral pulses - Normal – Intact
eg. Dorsalis pedis - Abnormal – Unequal – PVD, Embolism

II. Blood Pressure

- Physically & Mentally relax (5 min rest)
- Correct cuff size & correct level (2/3 of arm, Ht level)
*small cuff – higher BP and tight clothes
around arm or larger cuff – lower BP
- Palpation and auscultation method
*(+) of auscultation gap may cause wrong SBP
* Phase V, not Phase IV, is DBP
* SBP by palpation < SBP by auscultation
(~ 5-10 mmHg)
- If required - Standing BP if suspected postural
hypotension
BP in leg - prone, large cuff, popliteal artery
- Pulse pressure
Wide pulse pressure ( > 60 mmHg) *AR
 Narrow pulse pressure ( < 20 mmHg) *AS

III. JVP

- At 45o inclination position - Look from Rt side

- If pulsation (+), Confirm JVP by pressure at roof of the neck +/- Abdominojugular
reflex - Measure with 2 rulers - the vertical distance between the sternal angle and the
top of the venous column in IJV.
- Normal JVP ( Rt atrial pressure) - < 7 mmHg ( 9cmH20 ); i.e < 4 cm from sternal
angle > 4cm from sternal angle - raised JVP
IV. Precordium examination
Inspection
(1) Shape of precordium - Normal
AbN - bulging (chronic LV dilatation),
pectus excavatum, pectus carinatum
(pigeon chest)
(2) Apex beat - Visible or not
(3) Other pulsations - Diffused pulsation (LV dilated & impaired eg. AMI, CMP, VHD (regur:))
Epigastric pulsation (RVH)
(4) Scar - Midline sternotomy scar ( CABG / valve replacement)
 Left submammary scar (Surgical mitral valvotomy)
Infraclavicular scars (Pacemaker implantation)

Palpation

(1) Apex (if cannot feel apex beat, left lateral position)
- Site of apex - Normal - Lt 5th I.C.S within midclavicular line
- Displaced *MR, AR
- Character - Normal (briefly lift the palpating finger)
- Tapping (palpable loud 1st H.S i.e in MS) *MS
- Heaving (LVH) *MR, AR, AS
- Double apical impulse (HOCM)
+ Thrill +/- (palpable murmur - grade 4 & above) – systolic / diastolic
(2) Left parasternal edge - LPSH (RVH or SEOLA effect)
+ Thrill +/-
(3) Pulmonary area - Palpable P2 (pulmonary hypertension)
+ Thrill +/-
(4) Aortic area - Thrill +/-

Persussion (not routinely necessary)

(1) Cardiac dullness - Normal - 3rd - 4th Left ICS
- AbN - widen cardiac dullness (pericardial effusion)
obliterated dullness (emphysema) Auscultation
- 5 area
- aNymif; 4 aNymif; Bell aNymif; (low pitch sound eg. MS)
Position aNymif; (for diastolic murmur)
Radiation aNymif; (for systolic murmur)
 Resp: aNymif; ( Lt – exp:, Rt – insp:, increased murmur intensity)

(1) Heart sound

- S1 - Normal *(at apex of heart)* [d/t closure of M & T valves during ventricular systole]
- AbN intensity - Loud S1 *MS
Soft S1 *MR
Variable
- S2 - Normal *(at base of heart )* [d/t closure of A & P valves during ventricular
diastole]
- AbN intensity - Loud S2 ( A2/P2 ) *Loud P2 - pul: hypertension
Soft S2 ( A2/P2 ) *AR
- Split

With bell - S3 [d/t rapid ventricular filling d/r passive filling] - Systolic failure / Vol: overload
- S4 [d/t stiff ventricle & forceful atrial contractn d/r active filling ] - Severe press:
At apex
Overload

(2) Murmur (turbulent flow)

At Mitral area - Pan systolic murmur* *MR
(Apex) - Mid diastolic murmur* *MS
- Late systolic murmur (rare)
- Late diastolic murmur / Presystolic accentuation
At Tricus: area- Pan systolic murmur
- Mid diastolic murmur
At Aortic area - Ejection systolic murmur*/ Mid-systolic murmua *AS
. At Pul: area - Ejection systolic murmur / Mid-systolic murmua
- Continuous marchinery murmur
At LPSE - Pan systolic murmur
- Early diastolic murmur* *AR
 Systolic murmur – PSM, ESM, LSM
Diastolic murmur – MDM, EDM, LDM/Presystolic murmur or accentuation

(3) Added sounds - Ejection click (AS, PS)

- Opening snap (MS, TS)
- Mid systolic click (mitral prolapsed)
- Prosthetic valve sound
- Pericardial rub (pericarditis)

MS – loud S1, S2, MDM MS – loud S1, S2, OS, MDM +/- PA ( lub-ta-ta-roo )
MR – soft or absent S1, PSM, S2 MR – soft/absent S1, PSM, S2, +/-S3
MS, MR – soft or absent S1, PSM, S2, MDM MS, MR – soft or absent S1, PSM, S2, MDM, +/-S3
AS – S1, ESM, S2 AS – S1, EC, ESM, S2, +/-S4
AR – S1, soft or absent S2, EDM AR – S1, (+/-ESM). soft/absent S2, EDM
 *Murmur – area, name, timing, pitch, character, intensity (grading), radiation,
bell/diaphragm, position, changing with respiration
*Description of auscultatory finding
MS - At mitral area, loud S1 & normal S2; low pitch, rumbling, MDM is heard. It is
localized. intensity is Grade (3 or 4). It is best heard with the bell of the
stethoscope, esp:ly in left lateral position and increased intensity during expiration.
MR - At mitral area, soft S1 & normal S2; high pitch, blowing, PSM is heard. It radiates
to let axilla. Intensity is Grade (3 or 4). It is best heard with diaphragm of the
stethoscope & increased intensity during expiration.
AS - At aortic area, normal S1 & S2; high pitch, crescendo-decrescendo/harsh/rasping
musical ESM is heard. It radiates to carotids/neck. Intensity is Grade (3 or
4). It is best heard with diaphragm of stethoscope and increased intensity
during expiration.
AR - At LSPE, normal S1 & soft S2; high pitch, decrescendo/ bellowing EDM is
heard. It is localized (radiate to lower sternum and apex). Intensity is
Grade ( 3 or 4). It is best heard with diaphragm of the stethoscope, esp:ly
when leaning forward position and increased intensity during expiration.
V. Signs of HF
- Right HF - Pitting oedema, JVP, Tender hepatomegaly
- Left HF - Bilateral basal crepitations
*Sitting - EDM; Bilateral basal crepitation; Sacral oedema
*Abdominal exam: - liver, spleen (IE)

OTHER RELEVANT SYSTEM EXAM: – nervous system – hemiparesis for embolic stroke

DIAGNOSIS
(Multi)valvular Heart d/s, MS / MR / MSMR / MS,MR,AR /
MS,MR,AS,AR, most probably rheumatic origin
[ +/- HF, +/- IE, +/- AF, +/- pulmonary hypertension]

POINTS FOR DIAGNOSIS

MS - Precordial exam:
P - Apex - not displaced & tapping, Diastolic Thrill +/- at mitral area

A - S1 - loud, S2 - normal, MDM at mitral area especially in left lateral position

MR - Precordial exam:
P - Apex - displaced & heaving, Systolic Thrill +/- at mitral area

A - S1 - soft/(-), PSM at mitral area with radiation to left axilla, S2 – normal

MSMR ~ MR + MDM

AR - Pulse - High volume pulse, Collapsing pulse, (Peripheral signs of AR ......................)

- BP - Wide pulse pressure
- Precordial exam:
P - Apex - displaced & heaving, Diastolic Thrill +/- at LSE
A - S1 - normal, S2 - soft/(-), EDM at LSE especially in leaning forwards position

AS - Pulse - Low volume pulse, (Slowing rising carotid pulse)

- BP - Narrow pulse pressure
- Precordial exam:
P - Apex - not displaced & heaving, Systolic Thrill +/- at aortic area
A - S1 - normal, ESM at aortic area with radiation to carotid, S2 - soft/normal
ASAR Pulse & BP - reduce signs of AR, Pulsus bisferiens (Carotid)
Precordial exam: - AR + AS

OTHER IMPORTANT POINTS TO FIND OUT IN VALVULAR HEART DISEASES

Atrial Fibrillation – Irregularly irregular pulse + Pulsus deficit

Pul: hypertension – Palpable P2, Loud P2, (RVH - LPSH)
Signs of HF – Left HF – Tachycardia (m/b Pulsus alternans),
Triple/Gallop rhythm,
Bilateral basal crepitation
Right HF – Raised JVP,
Dependent pitting oedema,
Tender Hepatomegaly
Signs of IE – Fever, Anaemia, Tinge of Jaundice, Subconjunctival haemorrhage, Dental caries,
Clubbing, Splinter haemorrhage, Osler’s node, Janeway’s lesion, Petechiae,
Absent distal pulses (embolism), Splenomegaly
Changing or new murmur (seagull murmur)
Roth spots on fundoscopy

DISCUSSION

# Causes of Bradycardia
Sinus bradycardia
Sleep Sick sinus $
Trained athletes Acute ischaemia of SA node
Hypothyroid Cholestatic J+
Hypothermia Raised ICP
Drugs (beta blocker, verapamil, diltiazem, digoxin)
Bradyarrhythmias
2nd degree Heart block
Complete Ht block
# Causes of Tachycardia
Sinus tachycardia
Exercise Hyperthyroid
Pain Pheochromocytoma
Anxiety Anaemia
Fever Heart failure
 Drugs (sympathomimetics eg. beta2 agonist, vasodilators)
Tachyarrhythmias
SVT (Atrial or Juntional) Atrial flutter
Ventricular tachycardia Atrial fibrillation
# Causes of Regularly irregular pulse
Pulsus bigeminus 2nd degree heart block with 2:1 or 3:1 block

# Causes of Irregularly irregular pulse

Sinus arrhythmia Atrial fibrillation
Atrial extrasystoles/etopics Atrial flutter with variable response
Ventri: 2nd degree heart block with variable response
extrasystoles/etopics # Causes of
Atrial fibrillation
(1) CAD (including AMI) (6) Alcohol (11) Chest infection
(2) VHD esp. Rheu: mitral d/s (7) CMP (12) Pul: embolism
(3) Hypertension (8) Sick sinus $ (13) Congenital Ht d/s
(4) Cardiac failure (9) Myocarditis & pericarditis (14) Pheochromocytoma
(5) Hyperthyroid (10) Cardiothoracic surgery (15) Idiopathic Lone AF
# Causes of high volume / bounding / collapsing pulse
AR, PDA,
Hyperdynamic circulation (Anaemia, Fever, Hyperthyroid, Beri beri, Peripheral AV shunt,
Paget's d/s of bone, CO2 retension),
Physiological (Exercise, Pregnancy, Increased environmental temperature,
Advanced age) # Causes of low volume pulse
MS, AS
Constrictive pericarditis, Cardiac tamponade
Cardiac failure, Shock
PVD

# Special character of Arterial pulses

(1) Collapsing pulse - large vol: pulse characterized by short duration with rapid rise and rapid
fall, exaggerated by raising the pt's arm above the level of the heart
~ Causes - as above
(2) Plateau pulse / slow rising pulse - gradual upstroke to the pulse wave form and reduced peak
occurs late in systole and is often associated with a notch on uptake (nacrotic
pulse)
~ Causes - aortic stenosis
(3) Pulsus bisferiens - 2 systolic peaks separated by a distinct midsystolic dip. (Double pulse
palpable)
 ~ Causes - AS+AR, HOCM
(4) Pulsus alternan - regular alternate beats that are weak and strong ~ Causes -
severe myocardial failure and indicate poor prognosis
(when BP measuring, SBP vary from beat to beat by as much as 50 mmHg, PR↑ when
lowering cuff) (5) Pulsus paradoxus - It is actually an exaggeration of normal response.
SBP during expiration - SBP during inspiration = > 15 mmHg
~ Causes – A/c severe asthma, Cardiac temponade, Pericardial effusion,
Constrictive pericarditis (6) Pulsus bigeminus (coupling ectopics) – d/t premature ectopic
beats following every sinus beat.
~ Causes - digoxin toxicity
(7) Pulsus deficit - HR > radial pulse rate
~ Causes - AF, ectopics

# Causes of unequal pulses

- Subclavicular artery - stenosis, thrombosis, embolism, external compression - Cervical rib
$
- Vasculitis (Takayasu's d/s, Giant cell arteritis)
- Dissecting aortic aneurysm
- Bralock - Taussing shunt (anastomosis b/t pul: artery and subclavian artery in TOF )
- Peripheral vascular d/s, Trauma
# Causes of radio-femoral delay
- Coarctation of aorta
- Embolism in one iliac artery
- Leriche's $ (aortic occlusive d/s eg. Saddle embolisation at aortic bifurcation)
# Phases in BP measuring
Phase 1 = Korotkoff sounds appear
Phase 2 = Silent gap (disappear of sound) - may be absent
Phase 3 = Reappear of Korotkoff sound
Phase 4 = Korotkoff sounds become muffled
Phase 5 = disappear of sounds
# Classification of Hypertension (BHS classification)
# Causes of Hypertension
I. Primary hypertension ~ Essential Hypertension (>95%)
II. Secondary Hypertension (5%) *especially <40 yrs - young hypentension
A) Renal causes (Renal Hypertension)
(1) Renal vascular d/s – RAS (3) Polycystic kidney disease
(2) Parenchymal renal d/s e.g. GN (4) Chronic renal failure
B) Endocrine d/s
(1) Acromegaly (6) Cushing's $
(2) Thyrotoxicosis (7) Primary Hyperaldosteronism (Conn's $ ) - adenoma
(3) P' Hypothyroidism (8) Congenital adrenal hyperplasia
(4) Hyperparathyroidism (d/t 11- hydoxylase or 17-hydroxylase deficiency)
(Hypercalcaemia) (9) Liddle's $ ( inproper of Na+ channel)
(5) Pheochromocytoma (10) 11- -hydroxysteroid dehydrogenase deficiency
C) Coarctation of aorta
D) Toxins
- Alcohol
- Drugs - OC pills (estrogen), anabolic steroid, corticosteroid, NSAID,
carbenoxolone, Sympathomimetic drugs
E) Others
- Pre-eclampsia, Obesity, ICP
# Causes of postural hypotension (Drop in SBP > 20 mmHg or BP > 20/10 mmHg on standing)
Relative hypovolemia eg. excessive diuretic Rx
Sympathetic degeneration eg. DM, Parkinson'd/s, ageing
Drug therapy eg. vasodilater, antidepressants.
# Causes of wide pulse pressure - AR, PDA, Hyperdynamic circulation, Systolic HT in elderly
# Causes of narrow pulse pressure - AS, hypovolumia
# Haemodynamic effects of respiration
Inspiration Expiration
Pulse/heart rate Accelerates Slows
Systolic BP Falls (up to 10 mmHg) Rises
JVP Falls Rises
 Second heart sound Splits Fuses
# Differences b/t carotid and JVP
JVP Carotid
1) Rapid inward movement 1) Rapid outward movement
2) 2 peak per Ht beat 2)1 peak per Ht beat
3) Impalapable 3) Palpable
4) Pulsation ↓ by press: at root of neck 4) unaffected
5) Varies with resp: and position 5) Independent of resp: and position
6) Abdomino-/Hepato-jugular reflex (+) 6) (-)
# Causes of elevated JVP
(1) Rt Ht failure (5) Over infusion or excessive infusion of fluid
(2) Constrictive pericarditis (6) SVC obstruction (absent pulsation)
(3) Cardiac tamponade (7) Pulmonary embolism
(4) Renal d/s with salt and water retension
# Wave form of JVP

'a' wave - atrial systole, T valve open

'c' wave - closure of T valve, not normally visible
'x' desent - atrial relaxation, T valve closed
'v' wave - atrial filling during ventricular systole when T valve closed
(or) peak pressure in RA immediately prior to opening of T valve
'y' desent - ventricular filling (early atrial emptying), T valve open

# Abnormalities of JVP
'a' wave - (-) 'a' wave - AF
Giant 'a' wave - TS, RVH d/t PS, Pul: hypertension
Cannon wave - Irregular - complete Ht block, VT of ectopics (AV dissociation)
- Regular - junctional / nodal rhythm
'v' wave - Giant 'v' wave (or) Giant 'cv' wave - TR, Single chamber ventricular pacing
'y' wave - Steep / rapid 'y' descent - constrictive pericarditis, TR
Slow 'y' descent - TS
Friedreich's s/- - rapid fall and rapid rise again d/t shiff ventricle
- Causes - constrictive pericarditis, restrictive CMP
Kussmaul's s/- - Elevation of JVP during inspiration
- Causes - cardia tamponade, constrictive pericarditis
# Why use internal jugular vein and not external jugular vein
- No valves b/t Rt atrium and IJV
- EJV is more superficial and prominent, but it is prone to kinking and partial obstruction
as it transverses the deep fascia of neck
# Surface anatomy of IJV
- IJV enter the neck behind the mastoid process. It runs deep to the sternocleidomastoid m/s
before entering the thorax b/t the sternal and clavicular heads and can only be examined when
neck m/s are relaxed.
# Apex beat - Most lateral and inferior position where cardiac impulse can be left
- Common abnormalities of apex beat
Volume overload eg. MR, AR - displaced, active, heaving (rocking)
Pressure overload eg. AS - not displaced, significantly, heaving (thrusting)
Dyskinetic eg. IHD, aneurysm - displaced, incoordinate
- Causes of displaced apex beat
Cardiac causes - LV dilatation (d/w & lat:ly) - ↓contractility (heart failure); volume overload
- Destrocardia ( in Rt side)
Respiratory causes - Pleural effusion, Pneumothorax – to opposite side
Collapse – to same side
- Causes of heaving apex beat
LVH - pressure overload (hypertension,
AS), volume overload (AR, MR)
- Causes of Impalpable apex
Emphysema, obesity, thick muscular chest wall, pericardial effusion, pleural effusion #
Causes of LPSH
- RVH - pressure overload (pulmonary hypertension, PS), volume
overload (PR, TR)
Cor pulmonale (RVH +/- failure d/t d/s of lung, chest wall or pul: circulation)
- SEOLA effect in MR
# Causes of Abnormal S1
Loud S1 - ↑ CO / Stroke vol: (eg. Hyperdynamic circulation)
MS with mobile cusps
Short P-R interval
Atrial myxoma (rare)
Quiet S1 - ↓ CO/ poor left ventricular function,
MR
Prolong P-R interval (1st degree Ht block)
Variable intensity - AF, Extrasystole/ectopics, Complete Ht block
# Causes of Abnormal S2
Loud S2 - A2 - systemic hypertension
P2 - pulmonary hypertension
Quiet S2 - Low CO, AS, AR (A2)
PS (P2)
Split - Physiological split - during inspiration [A2P2]
Wide and fixed split - ASD
Wide and mobile split (widen in inspiration)
- RBBB, PS, Pulmonary hypertension, VSD, MR
Narrow/Reverse split (widen in expiration)
- LBBB, AS, Systemic hypertension, HOCM, ventricular pacemarker, PDA
# Causes of 3rd Ht sound
Physiological - Healthy young adults, athletes, pregnancy, fever
Pathological - Large, poorly contracting Left ventricle (systolic failure)
MR (volume overload)
# Causes of 4th Ht sound
Severe LVH d/t hypertension or AS (pressure overload)
HOCM, AMI
# Causes of PSM
MR, TR, VSD
Leaking mitral or tricuspid prosthesis
# Cause of MDM MS,
TS, Atrial myxoma
Carry Coomb's murmur (A/c RF), Austin Flint murmur (in severe AR)
Increased flow across M & T valve - e.g. ASD, severe TR (T valve);
VSD, PDA, severe MR (M valve)
# Causes of ESM
AS, PS, TOF (PS)
Flow murmur – ASD (Pul: flow murmur), AR (Aortic flow murmur), Anaemia
Innocent systolic murmur - fever, preg:, athletes, HOCM (obstruction at subclavicular region)
# Causes of EDM
AR, PR, Graham Steel murmur (in MS with severe pulmonary hypertension)
# Causes of LSM
Mitral valve prolapse, HOCM
# Causes of LDM / presystolic accentuation
MS
# Causes of continuous murmur (Machinery murmur)
PDA
AV fistulae (congenital, iatrogenic & collateral circulation in coarctation of aorta)
Mammary souffle ( d/t mammary blood flow in preg: and lactation)
 Venous hum in the neck ( d/t high venous flow in young children and severe anaemia)
# Features of benign or innocent Ht murmur
Soft, mid systolic (ESM), heard at left sternal edge, no radiation, no cardiac abnomality
# Intensity grading of murmur (Diastolic murmur 1 to 4)
(1) heard by an expert in optimum condition
(2) heard by a non expert in optimum condition
(3) easily heard; no thrill
(4) a loud murmur, with a thrill
(5) very loud, often heard over wide area, with thrill
(6) extremely loud, heard without stethoscope
# Peripheral signs of AR
(1) bounding pulse and collapsing pulse (water hammer pulse)
(2) dancing brachial pulse
(3) wide pulse pressure
(4) prominent carotid pulsation (Corrigan's s/-)
(5) head nodding (de Musset's s/-)
(6) pulsatile uvula (Muller's s/- )
(7) capillary pulsation in nail beds (Quinke's s/-)
(8) pistol shot murmur over femoral arteries (Traube's s/-)
(9) femoral diastolic murmur as blood flows backward in diastole (Durozieg' s/-)
(10) Lighthouse sign (blanching & flushing of forehead)
(11) Hill's sign - ≥ 20 mmHg difference in popliteal and brachial SBP, seen in chronic severe
AR. Considered to be artefact of sphygmomanometric lower limb pressure measurement
# Peripheral signs of TR
Giant 'cv' wave in JVP
Pulsatile liver
# Severity assessment in valvular heart d/s
Symptoms - -/s of HF
Signs - MS - duration of MDM increased, narrower the distance b/t S2 and O.S
MR - Apex - more heaving and displaced, S3
AS - narrower pulse pressure, soft S2 with narrow or reverse split, S4, Apex - heaving
AR - wide pulse pressure, soft S2, S3, duration of EDM increased, Austin-Flint murmur
# AR Vs PR - Intensity with respiration, Peripheral signs of AR
# MR Vs TR - Site, Radiation, Intensity with respiration, Peripheral signs of TR
# MSMR
MS dominant or MR dominant

Apex - not displaced - displaced

- tapping - heaving

S1 - loud - soft
S3 - (-) - (+)

# MS
loud S1 - mitral valve closure against high LA pressure (or) from distance
(-) in calcified mitral valve
O.S - forceful opening of mitral valve
(-) in calcified mitral valve
Presystolic accentuation - d/t vigorous LA contraction
(-) in AF
# Causes of Mitral Stenosis
Almost always Rheumatic in origin
Others causes
Congenital (Lutenbacher's $ -
MS + ASD), Heavy
calcification in elderly,
Prosthetic valve.
Mucopolysaccharidoses, Endocardial fibroelastosis,
Malignant carcinoid # Causes of Mitral Regurgitation Mitral valve
prolapse.
Dilatation of mitral valve ring (eg. Rheumatic fever, CAD, CMP)
*Functional Damage to valve cusps & chordae (eg. RHD, Infective
endocarditis) Damage to papillary m/s - MI, after Sx for MS.
*RF is principal cause of MR in countries where RF is common
# Causes of Aortic Stenosis
Infants, children, aldolescents - Congenital aortic stenosis
- Congenital subvalvular aortic stenosis
- Congenital supravalvular aortic stenosis
Young adult to middle aged - Calcification & Fibrosis of congenital bicuspid aortic valve
- Rheumatic aortic stenosis
Middle aged to Elderly - Senile degenerative aortic stenosis
- Calcification of bicuspid valve
- Rheumatic aortic stenosis
# Causes of Aortic Regurgitation
Congenital - Bicuspid valve or disproportionate cusps
Rheumatic disease
Infective endocarditis
Trauma
Aortic dilation (Marfan’s $, Aneurysm, Dissection of aorta, Syphilis, Ankylosing
spondylitis & other sero (-) spondarthritis)
Hypertension (functional)
# Causes of Tricuspid Stenosis
Rheumatic heart disease
Carcinoid syndrome (fibrosis)
# Causes of Tricuspid Regurgitation
Congenital – ASD, Ebstein’s anormaly
Rheumatic heart disease
Infective endocarditis
Carcinoid syndrome
Pulmonary hypertension
# Causes of Pulmonary Stenosis
Congenital – Tetralogy of Fallot, Turner’s $, Noonan’s $, Willaim’s $, Congenital
Rubella $ Rheumatic heart disease
Carcinoid syndrome
# Causes of Pulmonary Regurgitation
Pulmonary hypertension
# Auscultation in CVS
- Stethoscope - Inverted by French physician, Lannec
- Bell - emphasizes low pitch sound e.g. MDM, S4, (S3)
- Diaphragm - filters out these sounds an helps to identify high pitched sound
e.g. Normal Ht sounds (S1, S2), most systolic murmur, EDM, Added sounds (E.C, O.S, rub)
- Tubing should be - 25 cm long and thick enough to reduce external sound
- The auscultatory areas (mitral, tricuspid, pul: and aortic) do not correspond with surface
markings of heart valves, but are areas where transmitted sounds & murmurs are best heard.
- Right sided murmurs become louder on inspiration ( left ? - on expiration)
# Causes of unilateral and bilateral leg oedema
Unilateral
Deep vein thrombosis Soft tissue infection
Trauma Immobility, e.g. hemiplegia
Lymphatic obstruction
Bilateral
Heart failure
Hypoproteinaemia, e.g. nephrotic syndrome, kwashiorkor, cirrhosis
 Lymphatic obstruction, e.g. pelvic tumour, filariasis
Drugs, e.g. NSAIDs, nifedipine, amlodipine, fludrocortisone
Chronic venous insufficiency
Inferior vena caval obstruction
Thiamine deficiency (wet beriberi)
Milroy's d/s (unexplained lymphoedema at puberty; more common in females)
Immobility
# Signs of HF …………………….
# Signs of IE ……………………...