cardiac cycle and jvp

CARDIAC CYCLE AND JVP

DEPARTMENT OF MEDICINE M V J MEDICAL COLLEGE & R H CHAIRPERSION: PROF: DR .SADASHIVAIAH PRESENTATOR: DR.M.RAMESH BABU

OUT LINEINTRODUCTIONDEFINITIONANATOMY OF THE HEART NORMAL CADIAC CYCLE CAUSES OF ALTERATION IN THE CARDIAC CYCLEJVP DEFINITIONANATOMY AND PHYSIOLOGYMEASUREMENT OF JVPWAVE FORMS OF J VPABNORMAL WAVE FORMS AND CONDITION CAUSING IT

DEFINITION

The cardiac events that occur from the beginning of one heart beat to the beginning of the next are called the cardiac cycle.

CARDIAC CYCLE CONTINUED…. Each cycle is initiated by spontaneous

generation of an action potential in the sinus node.

This node is located in the superior lateral wall of the right atrium near the opening of the SVC,and the action potential travels from here to both atria and then through the a-v bundle into the ventricles.

CONDUCTION SYSTEM

SAN

ANT I/N TRACT OF BACHMAN

MIDDLE I/N TRACT OF

WENCKEBACH

POST I/N TRACT OF THOREL

AVN

LBB

RBB LAF LPF

BUNDLE OF HIS

PURKINJE SYSTEMMyocardium

CONTINUED.. There is a delay of more than 0.1 sec

during the passage of the cardiac impulse from the atria into the ventricles.

This allow the atria to contract ahead of ventricular contraction

The atria acts as a primer pumps for the ventricles.

AP IN A VENTRICULAR MUSCLE FIBRE

Phase 0 : rapid depolarization – opening of fast Na channels Phase 1 : rapid repolarisation – closure of Na channels Phase 2 : Plateau – slow prolonged opening of Ca channels Phase 3 : final repolarisation – rapid efflux of k+ channels Phase 4 : RMP (-85 to -90 mv) – opening of K channels

DIASTOLE AND SYSTOLE The caridac cycle consist of a period of relaxation

called diastole,during which the heart fills with the blood, fallowed by a period of contraction called systole.

Duration of cardiac cycle is the reciprocal of the heart rate.

If H.R -72/min, the duration of c. cycle -1/72 beats/min – about 0.0139 min/beat,or 0.833sec/beat

Duration of systole is 0.3 sec Duration of diastole is 0.5 sec

EFFECT OF HEART RATE ON DURATION OF CARDIAC CYCLE

When heart rate increases, the duration of cardiac cycle decreases , including the contraction and relaxation phases.

The period of systole decreases but not by as great a percentage as diastole.

The heart beating at a very fast rate does not remain relaxed along enough to allow complete filling of the cardiac chambers before the next contraction.

ATRIA AS PRIMER PUMPS About 80% of the blood flows directly

through the atria into the ventricles even before the atria contract.

Atrial contraction usally cause an addition 20% filling of the ventricles.

Normally atria has the capability of pumping 300-400% more blood than is required by the resting body.

CARDIAC CYCLE AND EVENTS

EVENTS OF CARDIAC CYCLE Filling of the ventricles during the

diastole. Period of rapid filling of the ventricles

lasts for about 1/3 rd of diastole. middle 1/3 rd only small amount of

blood normally flows into ventricles, during last 1/3 rd of diastole atria

contracts and give additional inflow for about 20%.

EMPTYING OF THE VENTRICLES DURING SYSTOLEPERIOD OF ISOVOLUMIC CONTRACTION

The ventricular pressure rises abruptly causing the a-v valves to close.

Additional 0.02-0.03sec is required for the ventricle to build up sufficient pressure to push the semilunar valves.

In this period contraction starts but no emptying. So called isovolumic or isometric contraction.

PERIOD OF EJECTION

When the L V pressure raises slightly > 80mm hg ( R V pressure >8mm hg ), the ventricular pressure pushes the semilunar valves open..

Period of rapid ejection –70% during first 1/3rd remaining 30% emptying during next 2/3rd –period of slow ejection.

PERIOD OF ISOMETRIC RELAXATION At the end of systole,ventricular relaxation

begins suddenly,allowing both the R & L intraventricular pressures to decrase rapidly.

Elevated pressures in the large arteries ,immediately push blood backward towards the ventricles, which snaps the semilunar valves to close.

Another 0.03-0.06sec requires for full relaxation of the ventricles (isovolumic relaxation).

A-v valves opens to begin a new cycle.

END DIASTOLIC VOLUME, END SYSTOLIC VOLUME & SYSTOLIC VOLUME OUTPUT

During diastole filling to about 110-120ml,this volume called end diastolic volume.

Ventricles emptying during systole ,the decreases to about 70ml- called the stroke volume output.

Remaining volume in each ventricle about 40-50ml is called end systolic volume.

The fraction of the end diastolic volume that is ejected is called the ejection fraction ~60%.

CONT… When heart contracts strongly, the ESV

can be decreased to as little as 10-20ml. When large amount of blood flow into the

ventricles during diastole, the ventricular EDV can become as great as 150-180ml in healthy heart.

By both Increasing EDV and decreasing ESV,the stroke volume output can be increased to more than double normal.

FUNCTIONS OF THE VALVES A.V. valves prevent blood flow from the

ventricles to atria during systole. Semilunar valves prevent blood flow from the

large arteries into ventricles during diastole. These valves open & closes passively,they

closes when back ward pressure gradient pushes, opens when the gradient forces blood in the forward direction

Thin A.V valves require no backflow, semilunar valves require rapid backflow for few mill.sec.

FUNCTIONS OF PAPILLARY MUSCLES

The papillary muscles contract when the ventricular walls contract, but they do not help the valves to close.

They pull the vanes of valves inward toward the ventricles to prevent their bulging.

If chorda tendinea ruptures the valves bulges far backward,results in severe or lethal cardiac incapacity.

SEMILUNAR VALVES

The high pressures in the arteries at the end of systole cause the semilunar valves to snap to the closed position.,much softer closer.

Smaller openings ,the ejection through the aortic and pulmanary valves is far greater than that through the a-v valves.

Strong yet pliable fibrous tissue base to withstand the extra physical stress.

VENTRICULAR PRESSURE- VOLUME LOOP

a – Ventricular filling 1 – Mitral valve closesb – isovol contraction 2 – Aortic valve opensc – ejection 3 – Aortic valve closesd – isovol relaxation 4 – Mitral valve opens

The filling phase moves along the end-diastolic pressure-volume relationship (EDPVR)

The slope of the EDPVR is the reciprocal of Ventricular Compliance

The maximal pressure that can be developed by the ventricle at any given left ventricular volume → end-systolic pressure-volume relationship (ESPVR), which represents the inotropic state.

↓ slope of ESPVR i.e. ↑ ESV

Compensatory rise in preload i.e. ↑ EDV

↓ SV

↓ EF

↓ Work

↑ EDP

Impaired ventricular contraction

SYSTOLIC DYSFUNCTION

Reduced venous return / compliance / relaxation (lusitropy)

↓ EDV

↓ SV

↓ or = EF

↓ Work

↑ EDP

DIASTOLIC DYSFUNCTION

Impaired LV filling

↓ EDV

↓ afterload ; ↓ ESV

↓ SV and CO

MITRAL STENOSIS

Afterload on LV ↓ Outflow resistance is ↓

EDV and EDP ↑

↑ SV

↓ EF

MITRAL REGURGITATION

High outflow resistance; LV emptying impaired

↑ Peak systolic pressure; ↑ afterload

↓ SV

↑ ESV

↑ EDV

AORTIC STENOSIS

No true isovolumetric relaxation

Blood from aorta to ventricle throughout diastole

↑ EDV

↑ SV (if no failure)

↑ ESV and ↓ SV in failure

AORTIC REGURGITATION

ECG TO THE CARDIAC CYCLE

ECG TO THE CARDIAC CYCLE

In Atrial systole Heart sounds - S 4 – pathological. Vibration of the ventricular wall during atrial contraction. Heard in ‘stiff’ ventricle like in hypertrophy and in elderly. Also heard in massive pulmonary embolism, cor pulmonale, TR In isometric contraction Heart Sounds – S1 : closure of the AV valves. Normally split as mitral valve closure preceeds tricuspid valve closure.

In Ejection Heart sounds – none In Isovolumic relaxation Heart sounds – S2 : closure of the

semilunar valves. Normally split because aortic valve closes slightly earlier than the pulmonary valve Heart sounds - S3 - Pathological in adults. Seen in dilated congestive heart failure, MI, MR, severe hypertension. Normal in children

DEFINITION Jugular Venous Pulse: defined as the oscillating top of

vertical column of blood in right IJV that reflects pressure changes in Right Atrium in cardiac cycle.

Jugular Venous Pressure: Vertical height of oscillating

column of blood.

WHY INTERNAL JUGULAR VEIN? IJV has a direct course to RA. IJV is anatomically closer to RA. IJV has no valves( Valves in EJV prevent

transmission of RA pressure) Vasoconstriction Secondary to

hypotension ( in CCF) can make EJV small and barely visible.

WHY RIGHT INTERNAL JUGULAR VEIN? Right jugular veins extend in an almost

straight line to superior vena cava, thus favouring transmission of the haemodynamic changes from the right atrium.

The left innominate vein is not in a straight line and may be kinked or compressed between Aortic Arch and sternum, by a dilated aorta, or by an aneurysm.

The patient should lie comfortably during the examination.

Clothing should be removed from the neck and upper thorax.

Patient reclining with head elevated 45 °

Neck should not be sharply flexed.

Examined effectively by shining a light tangentially across the neck.

There should not be any tight bands around abdomen

METHOD OF EXAMINATION

the level of venous pressure.

the type of venous wave pattern.

OBSERVATIONS MADE

Using a centimeter ruler, measure the vertical distance

between the angle of Louis (manubrio sternal joint) and the

highest level of jugular vein pulsation.

The upper limit of normal is 4 cm above the sternal angle,.

Add 5 cm to measure central venous pressure since right

atrium is 5 cm below the sternal angle. Normal CVP is < 9 cm H2O

THE LEVEL OF VENOUS PRESSURE

The level of venous pressure

The normal JVP reflects phasic pressure changes in the right atrium and consists of three positive waves and two negative troughs

Simultaneous palpation of the left carotid artery aids the examiner in relating the venous pulsations to the timing of the cardiac cycle.

NORMAL PATTERN OF THE JUGULAR VENOUS PULSE

Venous distension due to RA contraction Retrograde blood flow into SVC and IJV occurs just after the P of ECG,preceeds S1 Precede Carotid pulse

a wave

The x descent: is due to X Atrial relaxation X` Descent of the floor of the right

atrium during right ventricular systole. Begins during systole and ends before S2

The c wave: Occurs simultaneously with the carotid

pulse Artifact by Carotid pulsation Bulging of TV into RA during ICP

‘V’ WAVE

Rising right atrial pressure when blood flows into the right atrium during ventricular systole when the tricuspid valve is shut.

Synchronous with Carotid pulse Begins in late systole, Peaks after S2 and ends in

early diastole

The decline in right atrial pressure when the tricuspid valve reopens in early diastole.

It begins and ends during diastole.

Y DESCENT

The x descent occurs just prior to the second heart sound (during systole) , while the y descent occurs after the second heart sound (during diastole).

Normally X descent is more prominent than Y descent. Y descent is only sometimes seen during diastole. Descents are better seen than positive waves.

The a wave occurs just before the first sound or carotid pulse and has a sharp rise and fall.

The v wave occurs just after the arterial pulse and has a slower undulating pattern.

The c wave is never seen normally.

IDENTIFYING WAVE FORMS

A. Low jugular venous pressure

1. Hypovolaemia.

ABNORMALITIES OF JUGULAR VENOUS PULSE

1. Intravascular volume overload conditions Right heart failure Valvular Heart Disease with CCF Cardiomyopathy with CCF 2. Constrictive pericarditis.3. Pericardial effusion with tamponade

B. ELEVATED JUGULAR VENOUS PRESSURE

Increased

Resistance to RV Filling.

Tricuspid stenosisR Heart Failure PS PAH

ELEVATED “A” WAVE

Atrial-ventricular Dissociation

(atria contract against

a closed tricuspid valve)

Complete heart block

Ventricular tachycardia

Ventricular pacingJunctional rhythmJunctional

tachycardia.

CANNON “A” WAVE

ABSENT ‘A’ WAVE 1. Atrial fibrillation

1. Tricuspid regurgitation.2. Right ventricular failure.3. Restrictive cardiomyopathy.4. Cor Pulmonale

ELEVATED “V” WAVE

Absent X Decsent CV/ Regurgitant Wave Has a rounded contour

and a sustained peak Followed by a rapid

deep Y descent Amplitude of V

increases with inspiration.

Cause subtle motion of ear lobe with each heart beat

TRICUSPID REGURGITATION

ASDProminent X descent

followed by a large V wave

M ConfigurationIndicates a large L-R

shuntWith PAH A wave

becomes more prominent.

“A” WAVE EQUAL TO “V” WAVE

1. Cardiac tamponade.2. Constrictive Pericarditis3. RVMI4. Restrictive Cardiomyopathy5. Atrial septal defect

Blunted “x” descent1. Tricuspid regurgitation.2. Right atrial ischaemia

PROMINENT “X” DESCENT

PROMINENT “Y” DESCENT

1. Constrictive pericarditis. 2. Tricuspid regurgitation.

Absent “y” descent1. Cardiac tamponade.

2. Right ventricular infarction3. Restrictive Cardiomyopathy

Slow “y” descent1. Tricuspid stenosis.2. Right atrial myxoma.

M shaped contour Prominent X and Y descent (FRIEDREICH`SIGN) Y descent is prominent as ventricular filling is

unimpeded during early diastole. This is interrupted by a rapid raise in pressure as

the filling is impeded by constricting Pericardium The Ventriclar pressure curve exhibit Square Root

sign

CONSTRICTIVE PERICARDITIS.

A positive response is defined by a sustained rise of more than 3cm in jvp for at least 15s after release of the hand.

Most common cause of a positive test is RHF Positive test in: Borderline elevation of JVP Silent TR Latent RHF False positive: Fluid overload False Negative: SVC/IVC obstruction Budd Chiari syndrome Positive Test imply SVC and IVC are patent

ABDOMINO-JUGULAR REFLUX

Failure of decline in JVP during inspiration. Constrictive Pericarditis Severe RHF Restrictive Cardiomyopathy Tricuspid Stenosis

KUSSMAUL’S SIGN

BIBLIOGRAPHY Ganong’s textbook of Physiology Guyton’s book of Physiology Harrison’s principles of Internal

Medicine Textbook of Cardiology by Jonathan

Abraham Hurst textbook of Cardiology

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