Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

physical diagnosis > cardio2 > Flashcards

cardio2 Flashcards

1
Q

IJV vs carotid pulse

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

observing neck veins

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

calculating CVP

A

CVP=JVP+5

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

jugular venous pulse waveforms

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Kussmaul’s sign

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Lancisi’s sign

A
  • seen in tricuspid regurgitation
  • a and v waves merge into single wave (lose biphasic wave)
  • can flicker ear lobes
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

clinical presentation tricuspid regurgitation

A
  • lancisi’s sign

- hepatic pulsatility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

abdominojugular reflux

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

L ventricular heart failure presents with…

A
  • positive hepatojugular reflux
  • crackles
  • S3 gallop
  • lateral displacement of PMI
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

hyperkinetic pulses

A
  • if pulse pressure is normal: MR, VSD, HOCM

- if pulse pressure is widened: AR, anemia, pregnancy, thyrotoxicosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

pulsus parvus def

A

pulse of small amplitude

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

pulsus tardus def

A

pulse with slow upstroke

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

pulsus parvus + pulsus tardus

A

aortic stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

pulsus parvus but NO pulsus tardus

A

cardiomyopathy (dec. LV contraction)

mitral stenosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

pulsus bisferiens

A

double peaked pulse
assoc with single PMI
due to aortic regurgitation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

bifid pulse

A 
double peaked pulse
triple PMI (triple ripple)
due to hypertrophic obstructive cardiomyopathy (HOCM)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

normal location of PMI? where is it displaced in pressure load? volume load?

A
  • normal: L 5th ICS, MCL
  • volume load: displaced down and laterally (MR, AR, L heart failure)
  • pressure load: displaced up and medially (AS, HTN)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What does it mean if your the size of PMI is increased?

A

normally ~1cm
enlarged if >2.5cm
indicates L. Ventricular enlargement

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What does a double spiked PMI mean?

A

mitral regurg (due to palpable S3)

20
Q

When do you see a triple PMI?

A

HOCM

21
Q

Features of mitral regurg

A
  • double spiked PMI (palpable S3)
  • single spiked carotid pulse
  • PMI shifted down and laterally (vol. load)
  • holosystolic plateau murmur
22
Q

Features of aortic regurg

A
  • single spiked PMI
  • double spiked carotid pulse (pulsus bisferiens)
  • PMI shifted down and lateral (vol. load)
  • diastolic tapering murmur
23
Q

features of aortic stenosis

A

hypokinetic aortic pulse (pulsus parvus and tardus)

  • PMI shifted up and medially (pressure load)
  • palpable S4
24
Q

areas of auscultation for heart sounds

A
  • 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
25
Q

sequence of valve closure

A

MTAP (mitral–>tricuspid–>aortic–>pulmonic)

26
Q

auscultation S1

A
  • 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)
27
Q

auscultation S2

A
  • 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
28
Q

S2 splitting heard at apex

A

pulmonary hypertension

29
Q

tambour S2

A

loud and ringing S2 due to dilatation of aortic root (marfan’s syphilitic aortitis)

30
Q

mid-late systolic clicks

A

assoc. with MVP, most common congenital valvular disease

31
Q

auscultation S3

A
  • 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)
32
Q

auscultation S4

A
  • 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
33
Q

murmur

A

extra heart sound produced by turbulent blood flow through heart chambers
-can occur in systole or diastole but not both

34
Q

bruit

A

turbulent blood flow through an arteyr

most common causes: PDA, AV fistula

35
Q

Hum

A

turbulent blood flow through a vein

36
Q

diastolic murmur + systolic ejection flow murmur

A

severe aortic regurg

37
Q

systolic murmur and diastolic S3

A

severe mitral regurg

38
Q

murmur of mitral regurgitation

A

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
39
Q

murmur of aortic stenosis

A

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)

40
Q

how to differentiate mitral regurg and aortic stenosis?

A

hand grip maneuver (inc. afterload)

  • mumur of MR is enhanced
  • murmur of AS is softened
41
Q

murmur of aortic regurgitation

A

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
42
Q

strain valsalva or standing from squatting

A

dec. venous return:
MVP: inc. intensity murmur (moves earlier in systole and lengthens(
HOCM: inc. intensity murmur
AS: dec. intensity

43
Q

release valsalva or squatting

A

increased venous return
MVP: dec. intensity (moves later in systole and shortens
HOCM: dec. intensity
AS: inc .intensity

44
Q

murmur of pericardial friction rub

A
  • 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
45
Q

Frank’s sign

A

diagonal earlobe crease assoc. w/ CV disease

46
Q

Thrill

A

palpable shudder indicative of murmur with intensity >4/6

47
Q

causes of holosystolic murmurs

A

MR, TR, VSD

physical diagnosis (7 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions