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ECOS II final > Cardiac Lecture - Stewart > Flashcards

Cardiac Lecture - Stewart Flashcards

1
Q

Aortic stenosis presentations

A
  1. OLD valves are SAD : Syncope, Angina, Dyspnea
  2. Crescendo-Decrescendo (letter A)
  3. Calcified aortic valve
  4. Radiates UP to Carotids
  5. Increased intensity with Squatting Valsalva
  6. Decreased intensity Standing Valsalva
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2
Q

major cause of Tricuspid Regurgitation

associated type of murmur

A
  1. TRIscuspid hit the most by IV drugs (venous- TRI Drugs)

2. Holosystolic/pansystolic/plateau murmur (continuos throughout systole)

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3
Q

Aortic Regurgitation characteristics

A
  1. Early blowing diastolic murmur
  2. Connective tissue disorders
  3. Marfan Syndrome
  4. Head-blobbing
  5. Femoral Bruits (backwash->turbulence)
  6. Water-Hammer Pulse

ARR, there she blows early!

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4
Q

pathology and location of systolic ejection murmur

A

heard during systole at the apex of heart (5th ICS on MCL).
Mitral valve Regurgitation

murmur due to blood going to where it’s not supposed to go (backflow)

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5
Q

Mitral Stenosis Pathology

A
  1. Opening Snap (soon after S2, during distal as ventricle begins to fill)
  2. Rheumatic fever history (Rheumitral)
  3. OS is MS

opening snap is Mitral stenosis

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6
Q

Mitral Valve Prolapse (MVP)

A
  1. midsystolic-click to S2 (crescendo)
  2. young woman with psychiatric issues (anxiety)
  3. Myxematous (tumor) Valvular Pathology (MVP)

the MVP clicks in the Mid-dle of nowhere!!

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7
Q

pathology of systolic murmur

A

mitral regurgitation

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8
Q

Mitral Regurgitation

A
  1. Rheu-mitral (rheumatic cardiac disease)
  2. Radiates to Axilla (regurgitates to armpit)
  3. Best heard at Apex (it’s closer to axilla)
  4. Holosystolic (plateau)
  5. Loud/blowing

S1 lower than S2… since valve doesn’t fully close.. usually higher

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9
Q

effect of inspiration on murmur

A
  1. louder Right heart side murmur (T&P loud)
  2. increases preload
  3. increases intrathoracic pressure

R-In

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10
Q

effect of expiration on murmur

A
  1. Left heart louder (M&A) (L-expiration)
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11
Q

increase in preload on aortic murmur in HOCM

A

decreases aortic murmur

more blood volume and pressure push the ventricular septum away from the aortic outflow allowing blood to move easily

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12
Q

decrease in preload on aortic murmur in HOCM

A

increases aortic murmur

less blood to push septum away from outflow track thus an obstruction and disruption of blood flow

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13
Q

increased preload in MVP

A

improves mid-systolic click

allows the prolapsed valve leaflets to return to their normal orientation

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14
Q

MVP valves orientation under normal pressure

A

mitral valve leaflets prolapse into L. atria under normal pressure and cause a disruption in blood flow

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15
Q

HOCM pathophysiology

type of murmur

A
  • Loud aortic murmur
  • small left ventricle due to thickened left ventricular septum

septum underwent hypertrophy to increase workload

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16
Q

MVP pathophysiology under normal pressure

A

-blood leaks back into left atrium due to mitral valve prolapse under normal pressure

MVP with regurgitation

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17
Q

HOCM presentation

intensity of murmur with squat and standing valsalva

A

family history of sudden cardiac death at a young age

louder with decreased preload and afterload (stand)
softer with increased preload and afterload (squat)

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18
Q

4 possible causes of systolic murmurs

A

Aortic stenosis
Pulmonary stenosis
Mitral regurgitation
Tricuspid regurgitation

19
Q

+ HJR (Hepatic Jugular Reflux)

A
  • poorly compliant RV, RV failure (failing to stretch so blood backflows easily)
  • constrictive pericarditis
  • obstructive RV filling due to RA tumor/ TS

+VE: Blood builds up in jugular and is visible as they distend and pulsate for a longer time

distension disappears sooner in a healthy heart –> heart increases outflow in response to increased blood volume

20
Q

cause of Increased JVP

A
  • SVC obstruction
  • severe heart failure
  • constrictive pericarditis, cardiac tamponade, RV infarction
21
Q

V wave

A

Atrial filling / ventricular contraction

  • increasing volume and pressure and RA when TV is closed
22
Q

prominent V wave could mean

A
  • TR (backflow of blood into atria increases pressure)

- pulm hypertension (increase RA due to back-pressure)

23
Q

A wave

A

R. Atrial Contraction, TV opens. coincides with S1, precedes carotid pulsation

24
Q

Giant A wave

A
  • obstruction between RV AND RA (TV stenosis, RA myxoma)
  • Increased RV pressure (pulmonary stenosis)
  • recurrent pulm emboli
  • pulmonary hypertension
  • A-V dissociation (complete heart block, Ventricular Tachycardia)….(cannon a waves ) - RA contracts against the closed TV… In normal cases, Ventricle and A contraction shld be 1 after the other allowing TV to close and open but as long as there is no communication btwn the 2, there is continuous contraction on both ends while TV is closed
25
Q

c wave

A

backwash push by closure of TV during isovolumetric systole and by impact of carotid artery adjacent to JV

26
Q

X WAVE AND STEEP X WAVE

A

x-wave: passive atrial filling and atrial relaxation. blood flows into the RA from the cava and TV is closed

steep x: caridiac tamponade , constrictive pericarditis… making heart chamber unable to fully comply/stretch

27
Q

y wave

deep Y CAUSE
slow Y

A

rapid ventricular filling - open TV –RV diastole

deep Y (low Y pressure): severe TR 
slow: obstruction to RV filling (TS/ RA myxoma)
28
Q

S3

A

left atria fills the stiff, non-compliant left ventricle under high pressure

(LIKE trying to fill and already full ventricle)…more like applying brakes — failing ventricle

pathologic over 40 but physiologic in young chn/ young adults

Ken-Tuck-Y

29
Q

S4

A

Ten-Nes-See

atrial filling sound due to high pressure from SVC/IVC and pulm venous return

Hypotension, CAD, old infarction

normal in athelets

30
Q

loudest point of S1 and S2

A

S1: at the apex …Mitral valve (L.5th ICS at MCL)

S2: at the base (Aortic valve) right 2nd ICS at sternal border

remember base of heart is at the top

S1 marks beginning of systole s2: end

31
Q

splitting of S2 happens during

A

Inspiration (physiologic)

due to increased VR during insp. and more time need for rv to deliver blood to the lung –delayed P2/p-closure

32
Q

Tricuspid valve location

A

L. 4th ICS at L. Sternal Border

33
Q

what grade do you start hearing thrills

A

grade 4-6

34
Q

4 points to check pitting for edema

A

Behind medial malleolus
dorsum of foot
anterior tibia (shin)
sacrum

35
Q

blunted diaphragms in a chest x-ray indicates

A

effusion

36
Q

cause of pansystolic murmur on right and left

A

right
VSD
Tricuspid regurg

left
mitral valve regurg

37
Q

cause of mid-late diastolic murmur (right and left)

A

right:
ASD
Tricuspid stenosis

left:
mitral stenosis (presystolic crescendo)
38
Q

left sternal border early diastolic murmur

A

aortic/pulmonic regurg

39
Q

continuous murmurs

A

congenital and clinical conditions (not necessarily uniform but murmur is heard all the time)

40
Q

Ebb’s point is best place to hear which murmur

A

aortic regurgitation - soft, high-pitched, early diastolic decrescendo

(btwn pulmonic and mitral valve)

41
Q

best position to listen to AR and MS

A

AR: seated and leaning forward (ebb’s point)
MS: left lateral decubitus (apex, PMI , BELOW NIPPLE ) - belly of stetho

42
Q

Late Systolic Murmur patient

A

healthy. non-pathological

43
Q

Diastolic vs systolic murmur grades

A

diastolic - 4
systolic 6

both are easily heard at 3
no thrills in diastole

ECOS II final (9 decks)

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