Shit - Cardio Flashcards Preview

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Flashcards in Shit - Cardio Deck (134):
1

bulbus cordis

smooth parts of ventricles (outflow tract)

2

primitive atria/ventricles

trabeculated part

3

primitive pulmonary veins

smooth part of LA

4

right horn of sinus venosus

smooth part of RA = sinus venarum (just incorporated into the atrium)

5

Left horn of sinus venosus

Coronary sinus: delivers deO2 blood from the heart into the RA

6

Right common cardinal vein and right anterior cardinal veins

SVC

7

How do you form the Membrnaous interventricular septum

From endocardial cushion

grows off muscular ventricular septum to join aorticopulonary septum (after it spirals)

 

 

8

Role of the endocardial cusions:

1) separate the atria from ventricles

2) Contribute to atrial septation

3) contribute to the membranous interventricular septum

4) Make all the valves (A,P,T,M)

9

3 fetal shuts: name, vessels, bypasses what

Ductus venosus: umbilical vein into IVC; bypasses liver

 

Foramen ovale: RA to LA; bypasses lungs

 

Ductus arteriosis: deO2 SV blood from head down into RV into pulmonary artery --> jump to descending aorta; bypasses lungs. [gives less oxygenated blood to extremities]

10

Fate of PDA

Close naturally via increased O2 and decreased plaental prostaglandins

 

Rx to close = indomethacin (NSAID, decrease PG)

 

Rx to keep open = PGE1 and PGE2

11

Allantois (urachus) becomes:

Median umbilical ligament

12

Umbilical arteries become;

MediaL umbilical ligaments

13

umbilical vein becomes:

ligamentum teres = round ligament (within falciform)

14

Which artery differ in supply with right and left dominant?

Posterior descending

15

Most common coronary artery occluded 

LAD

16

Peak coronary flow in what part of cycle?

Early diastole

17

most posteriro part of heart?

Left atrium

18

Supply of AV and SA

RCA

19

CO = 

= HR x SV

= MAP/TPR

= rate of O2 consumption/(Arterial O2 - Venous O2)

20

MAP = 

= CO x TPR

 

= 2/3 diast + 1/3 syst.

21

PP = 

= systolic - diastolic

 

= propotional to SV (systolic = full of blood, diastolic = empty)

= inversely proportional to arterial compliance (more compliant = more room for blood = lower systolic pressure because not pushing as hard on expanded walls, but roughly the same diastolic pressure)

22

SV = 

 

EF = 

SV = EDV - ESV

 

EF = EDV - ESV / EDV

EF = 55%

23

If HR increases, what will give to keep up withteh HR

Diastole

Therefore CO decreases (problem with v. tach)

24

Increase in PP via:

(see head bobbing)

Hyperthyroidism (increases beta-adrenergic, increases systolic)

Aortic regurgitation (leak back decreases distolic; then more to shoot out increases systolic)

Aortic stiffening (isolated systolic hypertension in elderly)

Obstructive sleep apnea (􏰂sympathetic tone)

Exercise (transient) 

25

Decrease PP in:

Aortic stenosis - low S

Cardiogenic shock - low S

Cardiac tamponade - S and D equalize

Advanced heart failure (HF) - low S

26

Acidosis on contractility:

decreases

 

(H+ into cells, K+ out, increased Na//K; decreased Na//Ca)

27

ACE-I/ARB effect on preload and/or afterload

Decrease both:

Less AT-II on BV = vasodilation (arterial) = decreased afterload

Less aldosterone = less BV = decreased preload

28

Effects of systolic vs diastolic HF on EF

Systolic = decresed EF (<55%)

Diastolic = same EF (becasue same all relative to EDV; contractility is fine)

29

Resistance = 

 = 8 x viscosity x length /  πr^4

 

= P/CO

30

Effect of organectomy on resistance and CO

Total body runs in parallel (1/R + 1/R); invidivual organs run in series (R+R)

 

So remove an organ will INCREASE TPR.

CO = P/R

with no change in P, CO will DECREASE

31

Inotrophy graph

+ = catecholamines, digoxin

- = uncomensated HF, Narcotic OD

32

Volume/venous tone graph

+ = fluid infusion, SNS

- = acute bleed, spinal anesthesia

33

TPR graph

- = exercise, AV shunt

+ = pressors

34

S3

SLOSH-ing-in

During late systole, when the ventricles are relaxing and atria are passively filling them with 80% of total blood volume (y-descent)

 

Physiological with high BV i.e. kids, pregnancy

Pathological with mitral regurg, HF, dilated ventricles

35

S4

a-STIFF-wall

 

Atrial kick

 

When atria contract against still ventricle to get last 20% of blood in (a-wave); i.e. ventricular hypertrophy

36

wide splitting via:

Delayed right ventricle emptying, delaying pulmonary valve closure

- RBBB

- pulmonary stenosis

37

Fixed splitting seen in:

why?:

ASD

Because left to right shunt .: always more blood in right (atrial and) ventricular system .: always takes longer to close pulmonary valve

38

Paradoxical splitting:

Seen in:

When A closes after P, so when you breathe in and P closes later, they end up closing closer together paradoxically eliminating the split

(inspiration normally enhances splits)

 

Seen when aortic closes later:

- LBBB

- Aortic stenosis 

- HOCM

39

Where to listen for flow murmurs (physiological)

Pulonary and aortic areas

40

Aortic and pulonary regurg location:

left sternal boarder

41

hypertrophic cardiomyopathy: where to listen

left sternal boarder

42

Where to hear VSD and ASD

Tricuspid

43

Aortic regurg facts:

Diastolic, high-pitched, Blowing, Decrescendo

Associated with: (via inc. PP)

- Bounding (corrigan's) pulse

- quinke's sign = pulsating nails

- demuzzet's sign = head bobbing

- Muller's sign = uvula pulsation

44

Mitral stenosis facts:

Diastolic

Opening snap

rumbing

rheumatic fever

decreased S2-OS = increased severity

45

Aortic stenosis facts

- congenital, calcification, bicuspid

- Systolic, cesc-decres

- pulsus parvus et tardus (small and late)

- may have S4 from hypertrophy 

- may have quiet/no S2

- can get paradoxical splitting

- complications = ASC (angina, syncope, CHF)

46

mitral regurg

Holosystolic, blowing, high-pitched

radiate to axilla

via ischemia (MI), MVP, LV dilation, RHD, Endocarditis

47

TR

High-pitched, blowing, holosystolic

loudest at tricuspic area, radiates to right sternal boarder

caused by RV dilation (also RHD or endocarditis)

48

VSD

holosystolic, harsh

tricuspid area

49

PDA

Continuous and machine-like, loudest at S2

 

Hear at left infraclavicular area

50

Bedside maneuvers

51

SNS activity on SA and AV nodes:

SA = chronotropy (HR)

AV = dronotropy (conduction velocity)

52

high-pitched "blowing murmur"

Any regurg

53

T inversion

recent MI

54

ST segment 

flat = isoelectric = ventricles depolarized but not changing 

 

Depressed = stable angina or subendocardial infarct

 

Elevated = pizmetal angina or transmural infarct

55

U-wave

via hypokalemia or bradycardia

56

Hyperkalemia and hypercalcemia effects on ECG

Both: decrease QT

 

HyperK+ inreases rate of repolarization (T-wave higher)

Hyper Ca++ also increases rate of repolarization somehow...

57

Torsades:

Long QT myocytes can pass their depolarization (+ charge) off onto neigbouring cells with normal QT that are already repolarizes → normal QT cells fire again .: ventricle cells all firing at different times (disorganized) = torsades

 

can become v.fib when the excessive repolarizations organize into loops (re-entry circuits)

58

Torsades ppt factors:

congenital: romero-ward, jervell and lange-nielsen - K+ ion channel defects, risk of  SCD

Low K+, Mg++, Ca++

Drugs:

  • Antiarrytmics (Ia + III - K+ blockers)
  • antiBiotics (macro)
  • antiCychotics (haloperidol)
  • antiDepressants (TCA)
  • AntiEmetics (ondansetron)

59

Romero-ward

Dominant

60

Jervell and lange-neilson

Recessive and sensorineural deafness

61

Brugada: disease and Rx

Adian males

AD

ST elevation in V1-V3 with pseudo-right bundle branch block

Risk of v. tachyarythmias and SCD

Rx = ICD

62

Wolf-Parkinson-White

bundle of kent; ventricles fire early

DELTA-wave .: decreases PR, wide QRS

can lead to re-entrant circuits = SVT [accessory path repols, so if it get depolarized again from the bottom (via another part of the ventricle that is still depolarized) the signal will travel UP the bundle into the atria cause a SUPRAventricular tachycardia]

63

TAPRV

Pulmonary veins drain into right heart 

64

Congenital defects NEEDING other defects to survive:

Tranposition of great vessels (ASD, VSD, or PFO)

Tricuspid atresia (BOTH ASD and VSD)

TAPVR (ASD, sometimes PDA too)

65

Most common congenital defects: early and late cyanotic

Early = tetralogy

 

Late =  VSD > ASD > PDA

66

ASD stethoscope

loud S1, fixed wide splitting of S2

67

ASD types and frequency

Osteum secundum = MC and isolated

 

Ostium primum = less common, associated with other defects i.e. in Downs

68

machinelike murmur

PDA

69

Late differential cyanosis

PDA (cyanosis in lower extremities)

70

Eisenmenger triad

Late cyanosis, clubbing, polycythemia

71

FAS heart:

ASD, VSD, PDA, Tetrallogy

72

Rubella heart:

septal defects, PDA, pulmonary artery stenosis

73

Diabetic mom, fetal heart

Transposition of great vessels

74

Marfans heart

MVP, cystic medial degeneration (thoaric AA and disection), aortic regurg

75

Prenatal lithium

Ebstein anomaly: low tricuspid with small RV

76

williams syndrome heart

supravalvular aortic stenosis

77

HTN in young woman: name and histo

Fibromuscular dysplasia of renal artery; string of beads

78

corneal arcus

lipids in cornea

 

old = arcus sinilis

young = hyperlipidemia

79

Smooth muscle migration signals in AS

PDGF, FGF

80

AS most common in what arteries (descending order)

Abdominal aorta > coronaries > popliteal/femoral > carotids > vertebrals

81

Abdominal vs throracic aortic aneurism risk factors:

abdominal = AS

 

thoracic = HTN, bicuspid aortic, CT disease, 3' syphylis/temporal arteritis/takayasu

82

Unequal BP in arms with mediastinal widening = 

aortic disection

83

ST depression can mean:

Stable angina

Unstable angina (with T inversion)

MI (NSTEMI, subendocardial, with biomarkers)

84

ST elevation can mean:

Prizmetal angina (transient)

MI (STEMI, transmural, with cardiac markers)

85

Prizmetal triggers

Tobacco, cocaine, triptans, ergots

86

MC arteries in MI

LAD > RCA > L circumflex

87

Complications post-MI by time:

0-4h; 4-24h, 1-3d, 3-14d, 2w+

0-4h = arrythmyas, HF, cardiogenic shock

4-24h = arrythmyas, HF, cardiogenic shock

1-3d = postinfarcting fibrinous pericarditis (frictoin rub) 

3-14d = ruptures: tamponade, MR, VSD. pseudoaneurism via contained free-wall rupture

2+ weeks = real aneurism, Dresslers

88

contraction band: time and why

4-24h post-MI, via reperfusion injury

89

STEMI ECG

90

abnormal heart sounds in hypertrophic cardiomyopathy

S4

Systolic murmur (i.e. mitral regurg because can't close)

91

causes of restrictive/infiltrative cardiomyopathy; ECG

sarcoidosis, amyloidosis, hemochomatosis, Loefflers (endomyocardial with eosinophils), endocardio fibroelastosis (young kids)

 

Diastolic dysfunction, low voltage ECG despite thick mycardium

92

Drugs that decrease mortality in HF:

ACE-I, ARB, b-blockers, spironolactone, hydralazine (also improves s/s)

93

bernheim and reverse berhheim

bernheim = LVF → LV enlargement → pushing into RV → obstructs flow → RHF s/s (liver, JVP, edema) but NO pulmonary edema

 

reverse bernheim = RVF pushing on LV

94

strep viridans endocarditis:

subacute

abnormal/diseased valves

dental procedures

95

Valve type and endocarditis:

- normal

- damaged

- prosthetic

- colon cancer

normal = s. aureus

damaged = s. viridans (mutans, sanguis)

prosthetic = s. epidermidis

colon cancer = s. bovis

96

ECG of acute pericarditis + causes

Wide and elevated S-T and/or PR depression

 

Causes = idiopathic, infection, radiation, autoimmune, uremia, CV (acute STEMI or dressler), neoplasia 

97

Myxoma vs rhabdomyoma

Myxoma = LA, obstruct mitral, diastolic "tumour plop", ground substance

 

Rhabdomyomas = ventricles, kids, with tuberous sclerosis

98

Kussmal sign: what and causes

Inspiration doesnt transmit to heart, so JVP

 

Constrictive pericarditis, restrictive cardiomyopathies, right-sided heart tumours

99

R-R of 5 little ECG boxes =

60bpm (0.2)

100

rate vs rhythm

rate = SA/AV Rhythm = myocardial AP

101

Arrythmya of binge drinking

A fib

102

Arrythmia of hyperthyroidism

a fib

103

Sawtooth arrythmya

A flutter

104

Completely erratic arrhythmia; fate

V fib. Death without CPR and defibrillation

105

A fib vs. a flutter Rx

A fib = antithombotic, rate, rhythm, cardioversion. A flutter = catheter ablation

106

constant but prolonged P-R

1st degree block

107

Regularly irregular

2nd degree, Mobitz I/Wenchebach

108

Random dropped beats (no warning)

2nd degree, Mobitz II. Need pacemaker

109

No link between atria and ventricles

3rd degree block

110

Micro cause of 3rd degree block

Lyme

111

Baro-R affect 4 things:

Contractility, HR, VC, BP

112

Cushing reaction

Triad: respiratory depression, bradycardia, hypertension

 

all via increased ICP

113

PCWP =

LAP

114

PCWP > LV diastolic P

Mitral stenosis

115

Irregularly irregular

a fib, no discrete (lose) P-waves

116

A fib causes:

binge drinking, hypertension, CAD, RHD, HF, valve disease, hyperthyroidism

117

R-R of 5 little ECG boxes =

60bpm (0.2)

118

rate vs rhythm

rate = SA/AV Rhythm = myocardial AP

119

Arrythmya of binge drinking

A fib

120

Arrythmia of hyperthyroidism

a fib

121

Sawtooth arrythmya

A flutter

122

Completely erratic arrhythmia; fate

V fib. Death without CPR and defibrillation

123

A fib vs. a flutter Rx

A fib = antithombotic, rate, rhythm, cardioversion. A flutter = catheter ablation

124

constant but prolonged P-R

1st degree block

125

Regularly irregular

2nd degree, Mobitz I/Wenchebach

126

Random dropped beats (no warning)

2nd degree, Mobitz II. Need pacemaker

127

No link between atria and ventricles

3rd degree block

128

Micro cause of 3rd degree block

Lyme

129

Baro-R affect 4 things:

Contractility, HR, VC, BP

130

Cushing reaction

Triad: hypertension, bradycardia, respiratory depression

131

PCWP =

LAP

132

PCWP > LV diastolic P

Mitral stenosis

133

Irregularly irregular

a fib, no discrete (lose) P-waves

134

A fib causes:

binge drinking, hypertension, CAD, RHD, HF, valve disease, hyperthyroidism