cardio2 Flashcards
IJV vs carotid pulse
venous pulse: biphasic, varies with position (angle of recline), height falls on inspiration, non-palpable/collapsible, abdominal pressure displaces pulse upward
-carotid pulse: single sharp wave, palpable/non-compressible
observing neck veins
look at IJV (better than EJV)
- find meniscus: for normal patients, angle of recline is 30-45 degrees
- for patients with increased CVP, angle of recline is increased
- for patients with decreased CVP, angle of recline is decreased
calculating CVP
CVP=JVP+5
jugular venous pulse waveforms
A wave: R. atrial contraction (large A waves seen with tricuspid stenosis, pulmonic stenosis, pulmn HTN, 1st degree AV block, supraventricular tachycardia)
- X descent: R atrial relaxation
- V wave: R atrial filling (larve V waves seen with tricuspid regurgitation, constrictive pericarditis)
- Y descent: R atrial emptying/opening tricuspid valve
Kussmaul’s sign
- increased JVP with inspiration due to impaired R. ventricular fililng (normally dec. JVP on inspiration)
- Causes: constrictive pericarditis, restrictive cardiomyopathy, pericardial effusion, R. heart failure, cardiac tumor, tricuspid stenosis
Lancisi’s sign
- seen in tricuspid regurgitation
- a and v waves merge into single wave (lose biphasic wave)
- can flicker ear lobes
clinical presentation tricuspid regurgitation
- lancisi’s sign
- hepatic pulsatility
abdominojugular reflux
- if you see hepatic pulsatility but not lancisi’s sign, push on abdomen for 15 seconds–>positive if you see IJV bulge
- if patient is asymptomatic=R. ventricular failure
- if patient is symptomatic=biventricular heart failure
L ventricular heart failure presents with…
- positive hepatojugular reflux
- crackles
- S3 gallop
- lateral displacement of PMI
hyperkinetic pulses
- if pulse pressure is normal: MR, VSD, HOCM
- if pulse pressure is widened: AR, anemia, pregnancy, thyrotoxicosis
pulsus parvus def
pulse of small amplitude
pulsus tardus def
pulse with slow upstroke
pulsus parvus + pulsus tardus
aortic stenosis
pulsus parvus but NO pulsus tardus
cardiomyopathy (dec. LV contraction)
mitral stenosis
pulsus bisferiens
double peaked pulse
assoc with single PMI
due to aortic regurgitation
bifid pulse
double peaked pulse triple PMI (triple ripple) due to hypertrophic obstructive cardiomyopathy (HOCM)
normal location of PMI? where is it displaced in pressure load? volume load?
- normal: L 5th ICS, MCL
- volume load: displaced down and laterally (MR, AR, L heart failure)
- pressure load: displaced up and medially (AS, HTN)
What does it mean if your the size of PMI is increased?
normally ~1cm
enlarged if >2.5cm
indicates L. Ventricular enlargement
What does a double spiked PMI mean?
mitral regurg (due to palpable S3)
When do you see a triple PMI?
HOCM
Features of mitral regurg
- double spiked PMI (palpable S3)
- single spiked carotid pulse
- PMI shifted down and laterally (vol. load)
- holosystolic plateau murmur
Features of aortic regurg
- single spiked PMI
- double spiked carotid pulse (pulsus bisferiens)
- PMI shifted down and lateral (vol. load)
- diastolic tapering murmur
features of aortic stenosis
hypokinetic aortic pulse (pulsus parvus and tardus)
- PMI shifted up and medially (pressure load)
- palpable S4
areas of auscultation for heart sounds
- Aortic: R 2nd ICS, parasternal line
- Pulmonic: L 2nd ICS, parasternal
- Erb’s point: L 3rd ICS, parasternal (left ventciular outflow)
- Tricuspid: L 4th-5th ICS, parasternal
- M: L 5th ICS, MCL
sequence of valve closure
MTAP (mitral–>tricuspid–>aortic–>pulmonic)
auscultation S1
- caused by closure of AV valves
- best heard at apex
- clinical variable is intensity:
- inc. intensity when inc. thickness of AV valve (mitral stenosis 2/2 rheumatic fever), inc. separation b/t AV leaflets at onset of ventricular sysole (MS, or shortened PR interval)
auscultation S2
- due to closure of semilunar valves (pulmonic and aortic)
- best heard at base
- clinical parameter: splitting
- physiologic splitting: occurs on inspiration (delayed P2 and early A2); should only be heard over pulmonic area
- paradoxical splitting: occurs on expiration (delayed A2, A2 follows P2); due to aortic stenosis, hypertension, LV dysfx (MI, L bundle branch block)
- fixed splitting: occurs in both inspiration and expiration due to ASD
S2 splitting heard at apex
pulmonary hypertension
tambour S2
loud and ringing S2 due to dilatation of aortic root (marfan’s syphilitic aortitis)
mid-late systolic clicks
assoc. with MVP, most common congenital valvular disease
auscultation S3
- low pitched, soft early diastolic sound
- best heard with bell at apex in LLD position
- caused by rapid deceleration of blood against ventricular wall=vol-overloaded states
- young atheletes with bradycardia (physiologic S3)
- mitral regurg
- tricuspid regurg
- LV failure (presents with tachycardia=S3 gallop)
auscultation S4
- low pitched, soft, late-diastolic extra sound
- best heard with bell at apex with patient in LLD position
- caused by strong atrial contraction due to ventricular hypertrophy (stiff ventricle) which occurs in pressure overloaded states–aortic stenosis, hypertension, pulmonary hypertension
- S4 over tricuspid area: strong R atrial contraction, strong A wave in neck veins
- S4 over mitral area: strong L atrial contraction
- with tachycardia=S4 gallop
murmur
extra heart sound produced by turbulent blood flow through heart chambers
-can occur in systole or diastole but not both
bruit
turbulent blood flow through an arteyr
most common causes: PDA, AV fistula
Hum
turbulent blood flow through a vein
diastolic murmur + systolic ejection flow murmur
severe aortic regurg
systolic murmur and diastolic S3
severe mitral regurg
murmur of mitral regurgitation
Causes:
- dilatation of annulus fibrosus (heart failure)
- acquired mitral valve damage (rheumatic fever)
- MVP (mid-late systolic click)
- dysfunction papillary muscle (ischemia)
- rupture of chordae tendinae (infection)
Murmur: systolic
- loudest at apex
- plateau-shaped
- starts immediately after S1 and extends all the way to S2 (holosystolic)
- can radiate to L. axilla
- assoc. w/ palpable S3 in severe cases
murmur of aortic stenosis
valvular type most common
causes:
- congenital (bicuspid valve); pts <50
- degenerative/calcific valve disease (most common cause in US, elderly)
- rheumatic fever (most common cause worldwide)
murmur: systolic
- diamond shaped (crescendo-decrescendo)
- starts immediately after S1 and ends before S2
- can radiate to neck
- palpable S4 if severe
Gallavardin phenomenon: can be mistaken for mitral regurg when listening at apex (mitral area)
how to differentiate mitral regurg and aortic stenosis?
hand grip maneuver (inc. afterload)
- mumur of MR is enhanced
- murmur of AS is softened
murmur of aortic regurgitation
Causes:
- aortic valve damage (calcific aortic degeneration, rheumatic fever, congenital defect, infective endocarditis, trauma)
- aortic root dilatation (marfan’s syndomre, syphilis, degerative, aortic dissection)
- VSD
Murmur: diastolic
- best heard at Erb’s point (L. 3rd ICS parasternal line); patient sitting upright and leaning forward with held exhalation
- diastolic tapering murmur
- if sever can have systolic ejection flow murmur
strain valsalva or standing from squatting
dec. venous return:
MVP: inc. intensity murmur (moves earlier in systole and lengthens(
HOCM: inc. intensity murmur
AS: dec. intensity
release valsalva or squatting
increased venous return
MVP: dec. intensity (moves later in systole and shortens
HOCM: dec. intensity
AS: inc .intensity
murmur of pericardial friction rub
- caused by severe pericarditis
- scratching, squeaky, creaking, leathery, fleeting “noise”; spans both systole and diastole
- enhanced by held inspiration or expiration and sitting up and leaning forward
Frank’s sign
diagonal earlobe crease assoc. w/ CV disease
Thrill
palpable shudder indicative of murmur with intensity >4/6
causes of holosystolic murmurs
MR, TR, VSD
