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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

• JVP can b distinguished from carotid pulse– Visible but not palpable– Double wave– Decreased when inspired (Kussmaul;s

sign)– Hepatojugular reflux – Can be obliterate

• 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 waveTricuspid regurgitation

Thoracic aortic dissectionPathologyBlood splits aortic mediaChief complaint• Chest pain – tearing and

radiate to back• Hemiplegia (carotid artery)

paraplegia (spinal cord artery)• Unequal pulse or BP of arm• Acute limb ischaemiaIf dissection move upwardCause aortic regurgitation or inferior MITypeType A – involve ascending aortaType B – not involving ascending aorta

Mitral stenosis

SymptomshemoptysisSigns• 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)

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

• 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

• 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.

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.

Cor pulmonaleDefRight 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

SymptomsSOB, fatigue, Signs• Cynosis, polycythaemic• Tachycardia• Raised JVP• CHEST – heaving, pansystolic murmur (tricuspid

regurgitation), loud P2, early diastolic murmur• Hepatomegaly• Oedema

Investigation1. FBC – Hb, Hct (polycythaemia)2. ABG – PaO2 (hypoxia)3. CXR – right atrial & ventricular enlargement, prominent

pulmonary artery4. ECG – p pulmonale (R atrial enlargement), tall R wave in v1

and deep s wave in v6 (RT ventricular enlargement), R axis dev

Management 5. Treat the underlying cause6. Treat cardiac failure – diuretics such as furosemide7. Treat respiratory failure – give 24% o2 in acute phase. Chronic

-LTOT8. Venesection if hct >55%

Polycythaemia

Etiology• Primary – mutation of hemapoietic cells or progenitor

cells• Secondary – hypoxia, reduced cardiac outputPresenting features• Redness of palm and mucosal membrane eg conjunctiva• Murmur and clubbing- congenital heart ds• Splenomegaly- polycythaemia veraInvestigationHb, hct, red cell countManagement Venesection if hct >55% in cor pulmonale

• 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.