This document provides information on describing heart murmurs, heart sounds, and the jugular vein pressure (JVP) waveform. It discusses the timing, shape, location, and other characteristics of murmurs. It describes the first, second, third, and fourth heart sounds and what they indicate. It also explains how to assess the JVP waveform and what the different waves mean in terms of cardiac function. Causes of elevated JVP are outlined. Key information on cardiac auscultation and assessment of the JVP is summarized.

1. Heart Sounds, Valves
and JVP
Christiane Riedinger

2. How to describe a Murmur
● Timing Systolic, diastolic, early, late, middle
● Shape Constant, crescendo, decrescendo, crescendo-decrescendo
● Location Where best heard
● Radiation Sound radiates in the direction of the blood flow
● Intensity 1 = audible after longer auscultation
(Grades 2 = audible with stethoscope
acc. to 3 = audible
Levine) 4 = audible and palpable thrill
5 = audible with rim of stethoscope and palpable
6 = audible without stethoscope touching and palpable
● Pitch Low (press gently, bell), medium, high (press hard, diaphragm)
● Quality Harsh, musical, rumbling, blowing

3. Respiration and Murmurs
● Inspiration increases venous return to the RV/RA but decreases it to the
LV/LA
=> therefore inspiration accentuates R-sided murmurs => RIght
● Inspiration also causes an increase in the capacity of the pulmonary
circulation, leading to an increased ejection time and delayed closure of the
pulmonary valve. This accentuates a split 2nd heart sound.
● Expiration decreases venous return to the RV/RA but increases it to the
LV/LA
=> therefore expiration accentuates L-sided murmurs => LEft

4. Mnemonics
● PASS
○ Pulmonary and aortic stenosis are systolic
● PAID
○ Pulmonary and aortic insufficiency are diastolic
● Mitral and tricuspid murmurs are the opposite (MTIS and MTSD)

5. 1st Heart Sound
● At end of diastole
● Closure of atrioventricular valves:
○ Mitral
○ Tricuspid
● Split?

6. 2nd Heart Sound
● At end of systole
● Closure of semilunar valves
○ Aortic
○ Pulmonary
● Listen also in inspiration
● Split?
○ Inspiration accentuates split 2nd sound
○ Pathological cause: BBB where ventricle contracts later due to delayed
conduction
○ Wide-fixed split: split present but no accentuation with inspiration, sign of ASD
(ASD causes an increased amount of blood in the RV due to backflow from the
LA to the RA and therefore delayed closure of the pulmonary valve,
irrespective of respiration)
● Loud?
○ Pulmonary hypertension, shunts, PDA?, ASD, VSD, where is P2 loudest?

7. 3rd Heart Sound: S3/ventricular gallop
● Lub-de-dub (early diastolic sound, low f => use bell) I prefer lub-dub-de as diastolic
sound
● Normal up to 30y from blood rushing in during rapid ventricular filling phase
● Pathological: hypertrophied or dilated ventricle decelerates incoming blood
● Listen at apex (L-sided origin) or L sternal border (R-sided origin)
● Causes
○ Heart failure
○ MI
○ Cardiomyopathy
○ Hypertension (p↑)
○ Mitral/aortic regurge (V↑)
○ Constrictive pericarditis

8. 4th Heart Sound: S4 / atrial gallop
● Le-lub dub (end of diastole, low f => use bell)
● Atria contract into non-compliant ventricle
● Always pathological
● Hear at apex (L-sided origin) or L sternal border (R-
sided origin)
● Causes
○ Heart failure
○ MI
○ Cardiomyopathy
○ Hypertension

9. Where murmurs are heard loudest
2nd L intercostal space:
Pulmonary stenosis (R)
Ejection systolic
Radiates to back
Inferior to L clavicle:
Patent ductus arteriosus
Continuous machine-like murmur
3rd L intercostal space:
Aortic regurgitation (L)
High f blowing decrescendo
diastolic murmur
Potential S3 and Austin Flint
Apex:
Mitral regurgitation (L)
Pansystolic, radiates to axilla
2nd R intercostal space:
Aortic stenosis (L)
Ejection systolic
Radiates to L carotid
R costal margin:
Tricuspid regurgitation (R)
Crescendo-decrescendo or
rectangular systolic murmur
L costal margin:
Tricuspid stenosis (R)
Diasystolic murmur, opening snap?
Ventricular septal defect
Harsh pansystolic murmur
Diastolic - systolic - septal
(L) left-sided, (R) right-sided
Apex in lat. decubitus position:
Mitral stenosis (L)
Diastolic, low-pitched
decrescendo, opening snap
2nd L intercostal space:
Pulmonic regurgitation (L)
Decrescendo in early diastole

10. Note:
There is a separate table summarising murmurs in the download folder.

11. Pathogenesis of Valvular Disease
● Aortic stenosis => LV hypertrophy (P overload) => restrictive
cardiomyopathy / diastolic dysfunction => systolic dysfunction as muscle
bulk can’t keep up
(Can lead to syncope and sudden cardiac death)
● Aortic regurgitation => LV hypertrophy (P and V overload)
● Mitral stenosis => LA dilatation => pulmonary hypertension and oedema
=> RVH (even TR!)
LA dilatation causes problems in electrical conduction => arrhythmias
● Mitral regurgitation => LA dilatation and LV dysfunction

12. Cardiac Surgery: General Points
● Most common: Coronary artery bypass graft, aortic valve replacement, mitral valve
replacement
● Extensive pre-op tests, !active infection, dental check for valve surgery, imaging, …
● Cardiopulmonary bypass CPB
○ Heparinise
○ Venous cannula into RA/SVCandIVC to bypass circuit
○ Oxygenate, filter, adjust temperature
○ Return via aortic cannula in ascending aorta
○ Reversal of heparin with protamine
● Cardioplegia: intentional temporary cessation of cardiac activity, usually done with
intermittent or continuous K+ infusion into coronary arteries (anteriograde or
retrograde via coronary sinus vein), based on blood (for O2 delivery) or crystalloid to
prevent myocardial ischaemia

13. Cardiac Surgery: Post-operative Period
● Usually extubate within 6h, leave ITU within 24h, home within 5d
● Bloods, CXR and ECG on days 1,2,4,6
● First 6h
○ Heart function deteriorates due to ischaemia-reperfusion injury
○ Inotropic support and pacing
○ Diuresis > 1mL/kg/h
○ Decreasing of mediastinal bleeding
○ Increase insulin requirements
● Days 1-2
○ Wean inotropes, pacing, invasive monitoring lines
○ Remove chest drain after 2h no drainage
○ Mobilise after catheter and epidural removal
○ PCA morphine to oral analgesia
○ Aspirin, LMWH, furosemide
○ Start eating

14. Valve Surgery
● Repair (MV possible, e.g open valvotomy) vs replacement (AV repair unpredictable)
● Median sternotomy incision (R thoracotamy possible for MV)
● May perform CABG at the same time (although higher rate of complications)
● Patient on CPB
● Alternatives
○ TAVI: transcatheter aortic valve insertion
○ Percutaneous aortic valve replacement via femoral artery
○ Balloon valvuloplasty for stenosis
● Complications
○ Death
○ Stroke (from debris of calcified valve or when cannulating aorta)
○ Re-sternotomy for bleeding or tamponade
○ AF, heart block
○ Prosthetic endocarditis
○ Failure of valve, thrombosis or paravalvular leak
○ General
■ Chest infection
■ Wound infection

15. Options for Valve Replacements
● Repair (MV possible) vs replacement (AV repair unpredictable)
● Mechanical valve
○ Ceramic mono or bi-leaflet (St. Jude mechanical, Carbomedics), Ball-and-cage no longer
used (Starr Edwards)
○ Last forever but require warfarin so patient needs to be suitable
● Tissue valves (xenografts)
○ Mosaic, Perimount
○ Made from pig or horse pericardium suspended on a covered metal ring
○ Does not need warfarinisation
○ Last for 10-15y if AV or 6-10y MV, so 2nd operation needed of <65
○ Higher failure rate
○ For patients at risk of bleeding or child-bearing potential or older patients

16. JVP Waveforms
● Venous pressure as observed by internal jugular vein (between two heads of
sternocleidomastoid on medial aspect of clavicle, runs towards ear, ext. j.v. is mid-
clavicle superficial to SCM and towards angle of jaw)
● Gives information about RA pressure
● Pt has to sit at 45*
● ASSESS
○ H from angle of Louis / sternal angle
■ 7cm is normal, just about visible
■ >3.5/10? is raised
○ Character: pulsatile / non-pulsatile
○ If pulsatile: abnormal waves?
● If suspect it is so raised that above SCM sit patient up
● Check for hepatojugular reflux to observe if change can be elicited by compression (if
raised but no change => local obstruction vs. cardiac cause)

17. JVP Waveforms
● End of diastole
○ A = +ve pressure wave, atrial contraction/systole, back pressure
○ Raised in tricuspid stenosis or dominant in pulm.ht., Cannon A wave in complete
heart block when atria contract against closed tricuspid valve, absent in AF
● Systole
○ C = +ve pressure wave, ventricular contraction, back pressure from push
against tricuspid valve
○ X = -ve pressure wave, -ve pressure on tricuspid valve upon systolic ejection
causes drop of the wave
● Early diastole
○ V = +ve pressure wave, atrial filling against closed tricuspid valve
large if tricuspid incompetence during ventricular syst (tricuspid regurgitation)
○ Y = -ve pressure wave as tricuspid valve opens

18. Causes of raised JVP
● Fluid overload in heart failure
● Large A wave
○ Tricuspid stenosis
○ Right heart failure (atria contract more forcefully)
● Cannon A wave
○ Atrial flutter (asynchronous firing of atrial activity causing atrial contractions
against a closed tricuspid valve)
● Absent A waves
○ AF (no efficient atrial construction)
● Kussmaul sign
○ JVP rises with inspiration in pericardial effusion or tamponade as there is
high resistance to atrial filling
○ Normal: JVP decreases with inspiration as -ve thoracic pressure allows
easier emptying of the RA and flow towards the RA