Jugular venous pressure (JVP) refers to the height of blood in the jugular veins and provides information about right heart function. An elevated JVP indicates issues such as right heart failure, tricuspid valve problems, superior vena cava obstruction, or fluid overload. The JVP is assessed by looking for visibility, double waves, changes with inspiration, and hepatojugular reflux. Conditions that limit right ventricular filling can also raise JVP.

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3. Jugular venous pressure
• Jugular vein drain deO2 blood from head to
heart via sup vena cava
• Raised JVP indicates
– Right ventricular failure
– Tricuspid stenosis or regurgitation
– Sup vena cava obstruction
– Pericardial effusion / constrictive pericarditis
– Fluid overload
– Hyperdynamic circulation

4. • JVP can b distinguished from carotid pulse
– Visible but not palpable
– Double wave
– Decreased when inspired (Kussmaul;s sign)
– Hepatojugular reflux
– Can be obliterate

5. • Q why R side is choose instead of L? A: R is directedly drained into R atrium
• Any condition that cause limted right ventricular filling can cause raised JVP. For eg.
Consrictive pericarditis, cardiac temponade or R ventricular infarction. They cause
elevation of venous pressure which can is more marked on inspiration. Because
inpiration cause incr venous return
Dominant a wave
• Tricuspid stenosis
• Pulmonary stenosis
• Pulm hpt
Cannon a wave
• Complete heart block
Dominant v wave
Tricuspid regurgitation

6. Thoracic aortic dissection
Pathology
Blood splits aortic media
Chief complaint
• Chest pain – tearing and radiate
to back
• Hemiplegia (carotid artery)
paraplegia (spinal cord artery)
• Unequal pulse or BP of arm
• Acute limb ischaemia
If dissection move upward
Cause aortic regurgitation or inferior
MI
Type
Type A – involve ascending aorta
Type B – not involving ascending
aorta

7. Mitral stenosis
Symptoms
hemoptysis
Signs
• Mitral facies (mitral stenosis>red C.O.>vasoC)
• Apical pulse maybe laterally displaced or not
palpable (red L ventricullar filling)
• Palpable p2, raised JVP due to pulm hpt
• Auscultation :
– Loud s1 (loud closing of mitral leaf)
– Split s2, loud p2(open snap)
– Mid-diastolic murmur (low pitched, rumbling)

8. Aortic regurgitation
• Water-hammer pulse
– Collapsing pulse
– Raise arm vertically upward
– It feels like a tapping impulse transmitted
through bulk of muscle
– Pathophysiology : blood that pump to arm
during systole is emptied very quickly bck to
heart during diastole therefore causing a
palpable pulse

9. • Early diastolic murmur
• Austin flint murmur (An Austin Flint murmur is a mid-diastolic,
low-pitched rumbling heard at the apex. Austin Flint murmurs
occur in aortic regurgitation due to the vibration of the anterior
leaflet of the mitral valve as it is buffetted simultaneously by
the blood jets from the left atrium and the aorta.)
• Corrigan’s sign – prominent pulsation of carotid pulse
• Quicke’s sign – systolic plethora and diastolic blanching
• De musset sign – nod with each heart beat
• Muller sign – systolic pulsation of uvula
• Duroziez sign – diastolic murmur heard in femoral a with
finger pressing a distally

10. • Wide pulse pressure - The aortic valve separates the left
pumping chamber (ventricle) of the heart from the aorta, the
large blood vessel that supplies blood to the rest of your body.
When the aortic valve functions properly, it allows blood to be
pumped out of the heart and into the aorta and supports blood
pressure in the aorta between heartbeats.
• If the aortic valve doesn't close tightly (aortic regurgitation),
some of the blood that has already been pumped out of the
heart leaks back in (regurgitation). The heart tries to make up
for the problem by pumping out larger amounts of blood with
each heartbeat. This causes a decrease in diastolic blood
pressure in the aorta, resulting in an increase in pulse
pressure — the numeric difference between systolic and
diastolic pressure.

11. Aortic stenosis
• pulsus tardus et parvus, also pulsus parvus et
tardus, slow-rising pulse and anacrotic pulse
• a sign where, upon palpation, the pulse is weak/small
(parvus), and late (tardus) relative to its usually
expected character.
• It is seen in aortic valve stenosis.
• Typical findings in aortic stenosis :
– narrow pulse pressure
– left ventricular hypertrophy
– harsh late-peaking crescendo-decrescendo ejection systolic
murmur heard best at the right second intercostal space with
radiation to the carotid arteries
– delayed slow-rising carotid upstroke (pulsus parvus et
tardus)
– weak S2 and/or an S4 may also be noted.

13. Cor pulmonale
Def
Right heart failure caused by chr pulmonary arterial hypertension
Causes
• Lung
– COPD, asthma
– Bronchiectasis
– Fibrosis
– Lung resection
• Pulmonary vasculature
– Pulm embolism, pulm hpt
• Thoracic cage
– Scoliosis, kyphosis
• Neuromuscular ds
– Poliomyelitis
– Myasthenia gravis

14. Symptoms
SOB, fatigue,
Signs
• Cynosis, polycythaemic
• Tachycardia
• Raised JVP
• CHEST – heaving, pansystolic murmur (tricuspid
regurgitation), loud P2, early diastolic murmur
• Hepatomegaly
• Oedema

15. Investigation
1. FBC – Hb, Hct (polycythaemia)
2. ABG – PaO2 (hypoxia)
3. CXR – right atrial & ventricular enlargement, prominent
pulmonary artery
4. ECG – p pulmonale (R atrial enlargement), tall R wave in v1
and deep s wave in v6 (RT ventricular enlargement), R axis
dev
Management
1. Treat the underlying cause
2. Treat cardiac failure – diuretics such as furosemide
3. Treat respiratory failure – give 24% o2 in acute phase.
Chronic -LTOT
4. Venesection if hct >55%

16. Polycythaemia
Etiology
• Primary – mutation of hemapoietic cells or progenitor cells
• Secondary – hypoxia, reduced cardiac output
Presenting features
• Redness of palm and mucosal membrane eg conjunctiva
• Murmur and clubbing- congenital heart ds
• Splenomegaly- polycythaemia vera
Investigation
Hb, hct, red cell count
Management
Venesection if hct >55% in cor pulmonale

17. • History
• Increased red blood cell mass increases blood viscosity and decreases tissue perfusion,
potentially predisposing the patient to thrombosis.
• plethora or a ruddy complexion.
• If the polycythemia is secondary to hypoxia, as in venous-to-arterial shunts or
compromised lung and oxygenation, patients can also appear cyanotic.
• Symptoms may result from impaired circulation to the central nervous system, and patients
present with headaches, lethargy, and confusion or more serious presentations, such as
stroke and obtundation(altered level of conscious level).
• Congenital heart diseases manifest at birth or in early childhood. In some cases, a family
history of congenital heart disease may be present.
• Patients with familial hemoglobinopathies with increased oxygen affinity usually have a
family history of similar problems in several family members, although significant numbers
of patients with congenital polycythemia have no family history of similar disorders.[4]
• Chronic pruritus in the absence of a rash is more indicative of a primary myeloproliferative
disorder rather than secondary polycythemia.