CARDIOVASCULAR SYSTEM

CARDIAC CYCLE

VALVULAR EVENT (VALVES)

CARDIAC EVENTS ECG JVP(JUGULAR VENOUS PRESSURE CURVE)

Opening of A V valve End of isovolumetric relaxation phase"

End of T wave (phase b/w T wave

and new p wave)

V-Y descent"

Closure of AV valve End of diastole Beginning of

isovolumetric contraction

Later half of R wave

End of ‘X’ descent

Opening of semi lunar valve

End of isovolumetric contraction

ST segment Peak of 'C' wave

Closure of semi lunar valve

Beginning of isovolumetric relaxation phase

Beginning of diastole

Later half of T wave

JUGULAR VENOUS PULSE

A wave It is the positive presystolic wave produced by right atrial contraction.X descent 'A' wave is followed by the negative systolic wave the 'x' descent.

The x descent is produced due to atrial relaxationThe atrial relaxation is produced as a result of ventricular contraction.

C wave The x descent is interrupted by second positive wave the 'c' wave. It is produced by bulging of the tricuspid valve into the right atrium during RV isolvolumetric contraction.

V wave It is the positive systolic wave.It result from increase in the blood volume in the vena cava during systole, when the tricuspid valve is closed

Y descent Following the "v wave " this is a negative descending limb referred toAs the y descent or diastolic collapse.It is due to tricuspid valve opening and rapid inflow of blood into the right ventricle

ABNORMALITIES OF JVP

ABNORMALITIES OF ‘a’WAVE

GAINT ‘a’ wave CANON ‘a’ WAVE ABSENT ‘a’ WAVE

Obstruction at tricuspid valve

Tricuspid stenosis

Right atrial myxomas

Increase resistance to RV filling

Pul. HTN

Pul. Stenosis

Regular

Junctional rhythm

Irregular

Ventricular tachycardia

Ventricular ectopic

CHB

Atrial fibrillation

ABNORMALITIES OF ‘X’ DESCENT

Reversal of ‘X’ wave Tricuspid regurgitation

Accentuated ‘X’ wave Constrictive pericarditis

Cardiac tamponade

Restrictive cardiomyapathy

ABNORMALITIES OF ‘V’ WAVE

Accentuated ‘V’ wave: tricuspid regurgitation.

ABNORMALITIES OF ‘Y’ WAVE

Deep ‘Y’ decent Tricuspid regurgitation Constrictive pericarditis

Slow ‘Y’ decent Tricuspid stenosis Right atrial myxoma

HEPATOJUGULAR REFLUX OR ABDOMINOJUGULAR REFLEX This is done by applying firm pressure with the palm of the hand to the right upper quadrant of the

abdomen for 10-30 seconds with the patients breathing quietly while the jugular vein is observed. In normal subjects (Negative hepatojugular reflux)

Jugular venous pressure rises only transiently with rapid return to the baseline. Positive hepatojugular reflux (Left ventricular failure)

A positive abdominojugular reflux sign is defined by an increase in the jugular venous pressure of greater than 3 cm, sustained for greater than 15 seconds.

Conditions associated with abdominojugular reflux - Left ventricular failure (MC)

Right heart failure Constrictive pericarditis Right ventricular infarction Restrictive cardiomyopathy

KUSSMAUL'S SIGN Normally during inspiration there is a decrease in the mean jugular venous pressure as a result of the

increased venous return to the right sided chambers associated with the decrease in the intrathoracic pressures.

"In kussmaul's sign instead of decreasing, the J. V.P. increases during inspiration ". It indicates conditions where heart is unable to accept the increase in RV volume without a marked increase

in the filling pressure. Although kussmaul's sign was first described in constrictive pericarditis, its most common cause is severe

right sided heart failure regardless of etiology.Causes of kussmaul's sign are

Constrictive pericarditis Restrictive cardiomyopathy Right ventricular failure and infarction Tricuspid stenosis

PROMINENT ‘X’ & ‘Y’ DECENTFEATURE CARDIAC

TAMPONADECONSTRICTIVE PERICARDITIS

RESTRICTIVE CORDIOMYOPATHY

RVML

Prominent Y descent AbsentUsually present Rare

Rare

Prominent X descentPresent Usually present Present

Rare

ARTERIAL AND VENOUS PULSES

TYPES OF PULSES

PULSES ALTERNANS BISFERIENS PULSE(RADIAL ARTERY)

PULSUS PARADOXUS / PULSES NORMALIS AGGREGANS.

Regular alteration of pressure in pulse with regular rhythm (single peak)

Seen in VF May be seen in all

conditions leading to LVF

Toxic myocarditis

Two systolic peaks Aortic regurgitation± AS Hypertrophic

cardiomyopathy Pure AR

Normal decrease in systolic pressure during inspiration is accentuated

Seen in Pericardial tamponade S.V.C. obstruction COPD/Acute Severe Asthma Constrictive pericarditis Pulmonary embolism Hypovolemic shock

Dicrotic pulse Water hammer pulse (RADIAL ARTERY)Has two palpable waves one in systole and one in diastole.

Seen in – Dilated cardiomyopathy

The pulse strikes the palpating fingers with rapid force full jerks & quickly disappear

Aortic regurgitation

CARDIAC AUSCULTATION

HEART SOUNDS AND MURMURSFEATURE 1ST HEART

SOUND2ND HEART SOUND

3RD HEART SOUND

4TH HEART SOUND

Character High pitched (lower than S2) Slightly prolonged "tub"

High pitched (higher than S1) Shorter "dup"

Soft low pitched weak rumbling

Low pitched heart sound

Duration 0.14 second 0.1fsec 0.1 sec -Frequency 25-45 Hz 50 Hz - <20 Hz.Cause Sudden closure

of mitral & tricuspid valves

Closure of aortic & pulmonary valves

Rapid ventricular filling- d/t intrusting of blood from atria

Ventricular filling d/t atrial contraction causing intrusting of blood

Timing Start of ventricular systole (IVC)

Just after end of ventricular

Systole (IVR)

Beginning of middle third of diastole

Immediately before 1st

heart sound (presystolic)

Heard Better heard with Diaphragm

Better heard with Diaphragm

Better heard with the Bell

Better heard with the Bell

FIRST HEART SOUND (S1)

SOFT S1POOR CONDUCTION OF SOUND THROUGH CHEST WALL

DECREASE IN RATE OF LV PRESSURE DEVELOPMENT

PR INTERVAL & VELOCITY OF VALVE CLOSURE

MOBILITY OF VALVE

Obesity Emphysema Pleural effusion Pericardial

effusion

Myxoedema Cardiomyopathy Acute MI MR

Prolonged PR interval—1st degree heart block

Sever calcification of valve in MS

LOUD S1

Tachycardia Anemia Anxiety Fever. Short PR interval

At short PR interval the mitral valve leaflets are maximally separated by atrial contraction Increase A-V flow from high cardiac output e.g.

Thyrotoxicosis, Beriberi, A-V fistula

Increase AV flow due to Lt. to Rt. shunt e.g. ASD PDA, VSD

Prolonged A V filling due to A-V stenosis e.g. MS TS

FIRST HEART SOUND SPLITTINGSPLITTING OF FIRST HEART SOUND REVERSED SPLITTING OF THE FIRST HEART

SOUND Ebstein's anomaly Right bundle branch block (RBBB Delayed conduction of right ventricle -

LV pacing Ectopic beats

Idioventricular rhythms originating from left ventricle

Significant obstruction of the mitral valve (delay of closure of mitral valve)

Severe mitral stenosis Left atrial myxoma

Delay in the left ventricular contraction LBBB Pacing’s from right ventricle Ectopic beats and idioventricular rhythm

SECOND HEART SOUND (S2)PHYSIOLOGICAL SPLITTING OF S2

The increased volume within the right ventricle and decreased volume within the left ventricle during inspiration causes Prolonged P2 and Early A2 resulting in splitting of 2nd heart sound.

During inspiration (A2 and P2 are separated by more than 30 s) (A2---- 30ms —-P2)

During expiration The splitting disappearWIDE PHYSIOLOGICAL SPLITTING OF THE SECOND HEART SOUND

DELAYED PULMONARY CLOSURE Delayed electrical activation of the right ventricle

Complete RBBB (proximal type) Left ventricular paced beats Left ventricular ectopic beats

Prolonged right ventricular mechanical systole Acute massive pulmonary emboli. Pulmonary hypertension with right heart failure Pulmonary stenosis with intact septum.

Decreased impedance of pulmonary vascular bed Normotensive atrial septal defect Idiopathic dilatation of pulmonary artery Pulmonary stenosis Atrial septal defect

EARLY AORTIC CLOSURE Shortened left ventricular mechanical systole

Mitral regurgitation Ventricular septal defect

REVERSED SPLITTING OF S2DELAYED AORTIC CLOSURE EARLY PULMONARY CLOSURE

Delayed electrical activation of the left ventricle

Complete LBBB (proximal type) Right ventricular paced beat. Right ventricular ectopic beat Prolonged

left ventricular mechanical systole Left ventricular outflow tract obstruction Hypertensive cardiovascular disease Arteriosclerotic heart disease (Ischemia

and Angina) Decreased impedance of the systemic

vascular bed Postenotic dilatation of the Aorta

secondary to Aortic stenosis or regurgitation.

Patent ducts arteriosus

Early electrical activation of the right ventricle Wolff Parkinson White syndrome type B.

SINGLE S2CONDITION CAUSING

DELAYED AORTIC CLOSURE

CONDITION IN WHICH ONE COMPONENT OF S2 IS EITHER

ABSENT OR INAUDIBLE

INABILITY TO HEAR THE SOUND

All condition associated with delayed A2 can produce single S2 when splitting interval becomes <30ms

Truncus arteriosus Severe Tetralogy of Fallot Severe semi lunar valve

stenosis Pulmonary Artesia Tricuspid Artesia Eisenmenger's syndrome

Obesity Emphysema Plural effusion

**NOTE**

Causes of wide (fixed) split ASD (Most characteristic cause for wide fixed splitting) Pulmonic Stenosis Acute Right Heart Failure (Pulmonary Embolism)

THIRD HEART SOUND(S3) It is a low frequency sound It is a diastolic heart sound that occurs shortly after S2 It occurs during rapid filling of the ventricles (termination of rapid filling) It is best heard at the apex in the left lateral position It is better heard with the bell of the stethoscope

PHYSIOLOGIC S3 PATHOLOGIC S3

Children and young adults,

Atheletes, Pregnancy

Ventricular dysfunction - poor systolic function, increased end-diastolic and end-systolic volume, decreased ejection fraction, and high filling pressures.

Idiopathic dilated cardiomyopathy Ischemic heart disease Valvular heart disease Congenital heart disease Systemic and pulmonary hypertension

Excessively rapid early diastolic ventricular filling Hyperkinetic states Anemia Thyrotoxicosis Arteriovenous fistula Atrioventricular valve incompetence Left - to - right shunts (VSD, PDA and ASD) Restrictive myocardial or pericardial disease Constrictive pericarditis (Pericardial knock) Restrictive cardiomyopathy Hypertrophic cardiomyopathy

**NOTE** Congenital Heart Diseases associated with Loud S3

Ventricular septal Defect (VSD) Patent Ductus Arteriosus (PDA) A trial Septal Defect (A SD)

FOURTH HEART SOUND (S4) Fourth Heart sound occurs in association with an effective atrial contraction (It is presumably caused by inrush of blood into the ventricles when the atria contracts and hence it is also

called the ('Atrial Heart Sound') It is heard during the ventricular filling phase of the cardiac cycle (Presystolic heart sound) It is low pitched (frequency usually 20 cycle/sec or less- It is not audible to the unaided ear When audible the S4 is best heard with the bell of the stethoscope Loudest (Best heard) at the Left ventricular Apex when the patient is in left Lateral position It is accentuated by mild isotonic or isometric exercises in the supine position

Opening snapPericardial knockS3Tumour plop

S2

Mid systolic click

S4 S1

EC

CAUSES OF PATHOLOGICAL FOURTH HEART SOUNDFOURTH HEARTH SOUND (S4), ATRIAL DIASTOLIC GALLOP, AND PRESYSTOLIC GALLOP

Decreased ventricular compliance Ventricular hypertrophy

Left or right ventricular outflow obstruction Systemic or pulmonary hypertension Hypertrophic cardiomyopathy

Ischemic heart disease Angina pectoris Acute myocardial infarction Old myocardial infarction Ventricular aneurysm

Idiopathic dilated cardiomyopathy

Excessively rapid late diastolic filling secondary to Vigorous atrial systole Hyperkinetic states

Anemia Thyrotoxicosis

Arteriovenous fistula Acute atrioventricular valve incompetence

Arrhythmias Heart block

**NOTE** S4 is absent in atrial fibrillation

ADDED HEART SOUNDS

ADDED HEART SOUNDSDIASTOLIC SOUNDS SYSTOLIC SOUNDS

Opening snap S3 S4 Pericardial knock Tumour plop (atrial myxoma)

Ejection click Mid systolic click

LOCATION OF ADDED HEART SOUNDS IN SVSTOLE/DIASTOLE

SHORTLY AFTER S1

SHORTLY BEFORE S1

BETWEEN SI1& S2 SHORTLY AFTER S2

Ejection click Fourth heart sound

Midsystolic click Opening snap

Pericardial Knock

Tumor plop

S3

FEATURES OF ADDED SOUNDS

EJECTION CLICK OPENING SNAP PERICARDIAL KNOCK

TUMOR PLOP

Sharp,high pitched sound

Audible during early systole (Immediately after S1)

Seen in Aortic stenosis Pulmonary

stenosis Hypertension

Produced due to sudden opening of semilunar valve.

Brief high pitched sound.

Audible during early diastole

Seen in MS>TS

A S3 that is high pitched than normal

(S3 is low pitched)

Audible during early diastole

Seen in constrictive pericarditis

It is a low pitched sound

Audible during early or mid diastole

Seen in atrial myxoma.

OPENING SNAPFeatures

Brief high pitched sound Heard in early diastole (Ejection sound are heard in systole) It is usually due to stenosis of an (A. V.) most often mitral value. It follows second heart sound, by 0.05 to 0.12 sec. It is generally best heard at lower left sternal border and radiates well to the base of heart It is best heard during expiration The time interval between A2 and Os varies inversely with, the severity of M.S. It is followed by low pitched rumbling diastolic murmur

Opening snap indicates that M.S. is organic (andsignificant) Valve cusps are pliable High atroventiicular pressure gradient is present Severe, AR. MR, AF, SABE are absent.

CARDIAC MURMURS

CLASSIFICATION AND TYPES OF SYSTOLIC MURMURS HOLOSYSTOLIC PAN SYSTOLIC MURMURS

MIDSYSTOLIC MURMURS EJECTION SYSTOLIC

MURMURS

EARLY SYSTOLIC MURMURS

Begin with S1 and end after S2

VSD Mitral Regurgitation Tricuspid Regurgitation Aortopulmonary shunts

Starts shortly after S1 and ends before S2

Begin with first heart sound and end in midsystole

VSD Large VSD with pulmonary

hypertension V. small muscular VSD Tricuspid regurgitation in

absence of Pul. HTN Mitral regurgitation in a non

compliant left atrium as in

papillary muscle dysfunction

Aortic PulmonaryAS PSCOA Pul. HTNAneurysm ASDPDA Pul. Arterial dilatation

PHYSIOLOGICAL MANEUVERSPRELOAD – VENOUS RETURN AFTERLOAD

Rt heart sed – Inspiration

Valsalva – phase – 3 Passive leg raising Squatting

It heart sed – Expiration

Supine position Passive leg raising

Afterload sed Squatting Isometric hand grip Phenyl Ephrine

Afterload ¯ sed Amyl Nitrate

Systolic Murmurs

The intensity of all systolic murmur (Except MVP and HOCM) ¯ses -------------e ¯se preload ses -------------e se preload

¯ses -------------e se afterload ses -------------e ¯se afterload

But in HOCM and MVP these rules differs ¯se preload -----------ses intensity of murmur both in MVP and HOCM se Preload -----------¯ses intensity of murmur both in MVP and HOCM

So how are they differentiated they are differentiated based on afterload

se afterload ---------® murmur se in MVP® murmur ¯se in HOCM

¯se afterload ---------® murmur ¯se in MVP® murmur se in HOCM

**NOTE** In case of MVP - sed murmur means that mid systolic click occurs early and vice-versa

Low pitched- rumblingy diastolic murmur with 'Presystolic accentuation' heard best at the apex in left lateral recumbent position

CAREY COOMB'S MURMUR AND AUSTIN FLINT MURMUR CAREY COOMB'S MURMUR

Low pitched, delayed diastolic mitral murmur in association with Rheumatic fever AUSTIN FLINT MURMUR

Low pitched, delayed diastolic mitral murmur is association with severe chronic AR Common Condition Producing Acute MR Include

Rupture of chordaetendnae Papillary muscle dysfunction or rupture following MI Infective endocarditis

CONTINUOUS MURMURSCONTINOUS MURMUR

CAUSED BY BLOOD FLOWHIGH TO LOW PRESSURE

SHUNTLOCALISED ARTERIAL

OBSTRUCTION Venous humps Mammary soufflé Haemangioma Hyperthyroidisim Acute alcoholic

hepatitis Hyperemia of neoplasm

Systemic to pulmonary artery:

Patent ductus arteriosis Aorto pul. Window Truncus arteriosis Pul. Atresia Bronchiectasis Systemic artery to right

heart: ruptured sinus of valsalva coronary artery fistula venovenous shunts arterio venous shunts

Coarctation of arota. Branch pulmonary

stenosis. Carotid occlusion Celiac mesenteric

occlusion Renal occlusion

MURMUR OF MITRAL STENOSIS