Cardio Murmurs et EKGs Flashcards Preview

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Flashcards in Cardio Murmurs et EKGs Deck (57)
1

S1 heart sound

mitral and tricuspid valves close

2

S2 heart sound

aortic and pulmonary valves close

3

S3 heart sound causes?

early diastolic, occurs with increased filling pressures

cause: CHF, MR, pregnancy, children, dilated cardiomyopathy

4

S4 heart sound causes?

late diastolic, occurs with elevated atrial pressures

cause: ventricular hypertrophy

5

physiologic splitting of heart sounds

occurs during inspiration

6

when does fixed splitting of heart sounds occur?

ASD

7

paradoxical splitting of heart sounds causes?

LBBB, AS

8

wide splitting of heart sounds

RBBB, pulmonic stenosis

9

sound of patent ductus arteriosus? causes?

continuous machine-like murmur

congenital heart disease, congenital rubella

10

sound of ventricular septal defect?

holosystolic, harsh murmur at left sternal border

11

sound of mitral stenosis? causes?

sound: opening click w/ delayed diastolic rumbling (interval btwn S2 and click is inversely correlated w/ severity)

cause: rheumatic fever

12

sound of mitral valve prolapse? causes?

sound: mid systolic click followed by systolic crescendo murmur

cause: myxomatous dgeneration,  rheumatic fever (almost always), or chordae rupture

13

sound of mitral regurgitation? causes?

sound: holosystolic at apex with radiation to axilla (best heard in L decubitus position)

cause: MVP, LV dilation, ischemic heart disease, or rupture of chordae tendinae

14

sound of tricuspid regurgitation? causes?

holosytolic, radiates to R sternal border

cause: rheumatic fever, infective endocarditis, or things that cause RV dilation

15

sound of aortic stenosis? physical findings? causes?

sound: crescendo-descendo systolic ejection murmur (ejection click may be heard); loudest at 2nd right intercostal space (base) with radiation to carotids

parvus et tardus - pulses are weak w/ a delayed peak

cause: aortic sclerosis (age-related), bicuspid aortic valve

16

sound of aortic regurgitation? physical findings? causes?

sound: diastolic decrescendo murmur

PE: bounding pulses and head bobbing

causes: bicuspid aortic valve, aortic root dilation, endocarditis, rheumatic fever, SLE, syphilis

17

purpose of hand grip?

increase TPR (more remains in LV)

18

purpose of valsalva and standing?

decrease VR (less blood in heart's circuit)

19

purpose of inspiration vs expiration?

Inspiration - increase VR (more enters RA/RV)

Expiration - increase flow to LA from pulmonary circuit

20

purpose of rapid squatting vs prolonged squatting?

rapid: increase VR, increase preload

prolonged: increase afterload

21

what increases intensity of AS? decreases?

increase: rapid squatting

decrease: hand grip, valsalva

22

what increases intensity of MR? decreases?

increases: anything that increases TPR: hand grip, squatting

decreases: valsalva

23

what increases intensity of MS? decreases?

increase: expiration (increase LA return from pulmonic circulation)

decrease: valsalva

24

what increases intensity of VSD

increase: hand grip (to increase afterload)

decrease: valsalva

25

what increases intensity of AR? decreases?

increase: hand grip 

decrease: vasodilators, valsalva

26

what increases intensity of MVP? decrease?

increase: handgrip, squatting (increase TPR; later onset of click/murmur)

decrease: valsalva, standing (decrease VR; earlier onset of click/murmur)

27

what increases the intensity of R heart sounds?

inspiration

28

what increases intensity of tricuspid regurgitation? decreases?

increase: inspiration (maneuvers that increase RA return)

decrease: valsalva

29

type of arrhythmia?

at risk for?

trmt?

a-fib

  • Irregularly irregular
  • Ø P waves in between irregularly spaced QRS complexes

At risk of: Atrial stasis, thromboembolic stroke

Trmt:

  • Rate control
  • Anti-coagulation
  • Pharmacological or electrical cardioversion

30

type of arrhythmia?

trmt?

a-flutter

Rapid succession of identical back-to-back atrial depolarization waves

Trmt:

  • Class IA, IC, or III (slows down atrial contraction so that the waves can collide and cancel out, and the SA node can take over)
  • ß blockers or Ca channel blockres
  • catheter ablation

31

type of arrhythmia?

v-fib

Ø identifiable waves

at risk for: death - fatal

trmt: CPR and defibrillation

 

 

32

type of arrhythmia?

AV - 1st degree

PR interval is prolonged

33

type of arrhythmia?

AV - 2nd deg block - mobitz I

Progressive lengthening of the PR interval until a beat is dropped (P wave not followed by a QRS complex)

34

type of arrhythmia?

At risk for?

Treatment?

AV block - 2nd degree mobitz II

Dropped beats not preceded by a change in the length of the PR interval (2:1 block)



 

At risk for: progression to a 3rd degree block

Trmt: Pacemaker

 

 

35

type of arrhythmia?

trmt?

AV block - 3rd deg

Atria and ventricles beat independently of one another (no relationship between P waves and QRS complexes; atrial rate >> ventricular rate)

Trmt: Pacemaker

36

ventricular depolarization

phase 0

phase 1

phase 2

phase 3

phase 4

ventricular depolarization

phase 0 = rapid upstroke = VG Na open -> influx 

phase 1 = VG K open -> efflux

phase 2 = plateau = VG Ca open -> influx  (balances K efflux)

phase 3 = repolarization = more VG K open; VG Ca close 

phase 4 = resting potential (due to high K permeability)

37

SA depolarization

phase 0

phase 1

phase 2

phase 3

phase 4

phase 0 = upstroke = VG Ca open -> influx; VG Na inactivate 

phase 1 = does not exist

phase 2 = does not exist

phase 3 = repolarziation = VG K open, VG Ca close

phase 4 = If Na open -> Na conductance increases = determines HR

38

P wave

atrial depolarization

39

PR  interval 

conduction through AV node

40

QRS complex

ventricular depolarization

41

QT interval

mechnical contraction of the ventricles

42

T wave

 

inverted T wave?

ventricular repolarization 

Inversion may indicate recent MI

43

ST segment

isoelectric; ventricles depolarizsed

44

U wave

hypokalemia, bradycardia

45

Some Risky Meds Can Prolong QT

what are they?

Some Risky Meds Can Prolong QT

Sotalol

Risperidone

Macrolides

Chloroquine

Protease inhibitors (-navir)

Quinidine (Class Ia, III)

Thiazides

46

Romano-Ward Syndrome

AD, congenital QT syndrome - K channel defect 

risk of sudden death due to torsades (otherwise healthy young individual)

ø deafness

47

Jervell and Lange-Nielsen Syndrome

AR, congenital QT syndrome - K channel defect 

risk of sudden death due to torsades (otherwise healthy young individual)

Sensorineural deafness

did you HEAR about the Nielsen Ratings for Jekell & hyde?

48

3 holosystolic heart mumurs

what would accentuate these mumurs?

 

  • TR - increase in intensity during inspiration (more VR to R heart)
  • MR - increase in tensity with squatting/handgrip (more fluid remains in LV)
  • VSD (more fluid remains in LV)

49

type of murmur heard with hypertrophic cardiomyopathy

almost always associated w/ mitral regurg 2˚ to impaired mitral valve closure, therefore one would hear a systolic mumur

50

diastolic mumur best heard at the R sternal border is indicative of...

diastolic mumur best heard at the L sternal border is indicative of...

both are aortic regurgitation

R = due to aortic root dilation

L = bicuspid aortic valve?? not sure..but it is a common site to be heard

51

52

delta wave

Woff-Parkinson White Syndrome

caused by an abnormal fast accessory conduction pathway from A -> V, thereby passing the pace-determining step (AV node)

ventricles begin to depolarize earlier -> delta wave w/ shortened PR interval on ECG

may result in a reentry circuit -> supraventricular tachycardia

53

STEMI in I, aVL leads

lateral wall - LCX

54

STEMI in V1-V4 leads

anterior wall (LAD)

55

STEMI in II, III aVF leads 

inferior wall (RCA)

may cause sinus node dysfunction

56

STEMI in V1, V2 leads

anteroseptal (LAD)

infranodal Mobitz type II second deg or third deg block would be possible

57

STEMI in V4-V6 leads

anterolateral  wall (LAD or LCX)