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First Aid Stuff I Don't Know > Vol. III - Cardiovascular and Pharm > Flashcards

Vol. III - Cardiovascular and Pharm Flashcards

1
Q

role of diuretics in HF

A

symptom management

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2
Q

high pitched “blowing” early diastolic decrescendo

A

aortic regurgitation

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3
Q

Left horn of sinus venosus becomes

A

coronary sinus

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4
Q

Use of Class IB anti-arrhythmics

A

Acute ventricular arrhythmias esp post MI

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5
Q

How do we prevent cerebral vasospasm in subarachnoid hemorrhage

A

Nimodipine

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6
Q

Class 3 anti-arrhythmic mechanism

A

K channel blockers –> increased Ap duration, ERP, and QT interval

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7
Q

Fixed splitting is heard in

A

ASD

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8
Q

3rd aortic arch becomes

A

Common carotid

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9
Q

treatment for primary hypertension

A

Thiazide diuretics, ACE-i/ARBs, Ca channel blockers

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10
Q

Pathology 2-several weeks post MI

A

contracted scar is complete

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11
Q

Continuous machine like murmur, loudest at S2

A

patent ductus arteriosus

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12
Q

Primitive pulmonary vein becomes

A

smooth part of left atrium

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13
Q

Causes of tricuspid regurgitation

A

RV dilation and Rheumatic fever

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14
Q

Drug induced long QT –> Torsades risk

A

ABCDEF: antiArrhythmics (Ia and III), antiBiotics (macrolides and fluorquinolones), Anti”C”ychotics (haloperidol, ziprasidone), antiDepressants (TCAs), antiEmetics (odansetron), antiFungals (azoles)

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15
Q

6th aortic arch becomes

A

proximal pulmonary arteries and ductus arteriosus

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16
Q

Abnormalities associates with failure of neural crest migration

A

Transposition of the great vessels
Tetralogy of Fallot
Persistent truncus arteriosis

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17
Q

Causes of mitral regurgitation

A

Ischemic heart disease post mI, LV dilation, Rheumatic fever

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18
Q

systolic crescendo-decrescendo that radiates to the carotids, loudest at base of heart

A

Aortic stenosis

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19
Q

Hypertrophic cardiomyopathy findings

A

S4, systolic murmur, possible mitral regurg

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20
Q

Frequency of left to right sunts

A

VSD > ASD > PDA

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21
Q

Pathology 1-3 days post MI

A

Coagulative necrosis and acute inflammation with neutrophils

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22
Q

late systolic crescendo with mid-systolic click, best heard over apex

A

Mitral valve prolapse

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23
Q

Opening snap followed by mid to late diastolic rumble

A

mitral stenosis

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24
Q

pacemaker action potential phases

A

0: voltage gated Ca
3: repolarization via K efflux
4: spontaneous depolarization b/c of funny Na/K channels

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25
Q

Things that increase contractility

A

Beta 1 activation by cathecholamines, increased Ca, decreased extracellular Na, Digoxin

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26
Q

right horn of sinus venosus becomes

A

smooth part of the right atrium

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27
Q

cardiovascular complication of syphilis

A

aortic atrophy and dilation, can lead to calcification

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28
Q

treatment for htn with diabetes

A

ACE-i/ARBs first line, Ca channel blockers, thiazides, Beta blockers (can mask hypoglycemia though)

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29
Q

Pathology 3-14 days post MI

A

macrophage infiltration followed by granulation tissue at the margins

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30
Q

Class IC anti-arrhythmics

A

Flecainide, propafenone

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31
Q

Use of Class IA anti-arrhythmics

A

both atrial and ventricular, esp. SVT and VT

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32
Q

2nd aortic arch becomes

A

Stapedial and hyoid arteries

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33
Q

Class IA anti-arrhythmics

A

Quinidine, procainamide, disopyramide

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34
Q

Pericardium is innervated by

A

Phrenic nerve

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35
Q

Fick principle

A

CO = rate of O2 consumption / (arterial O2 content - venous O2 content)

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36
Q

Rheumatic fever pathogenesis

A

Type II hypersensitivity - Ab to M protein cross react with self antigen, often myosin

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37
Q

Use of Class IC anti-arrhythmics

A

SVT, including afib, contraindicated post MI

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38
Q

Paradoxical splitting is heard in

A

Conditions that delay aortic valve closure (aortic stenosis and left bundle branch block)

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39
Q

Treatment for Torsades de pointes

A

magnesium sulfate

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40
Q

Dilated cardiomyopathy findings

A

HF, S3, systolic regurg murmur

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41
Q

Conduction pathway

A

SA node –> atria –> AV node –> bundle of His –> bundle branches –> purkinje fibers –> ventricles

42
Q

Tetralogy of Fallot

A

most common cause of early childhood cyanosis

PROVe: Pulmonary stenosis, RVH, Overriding aorta, VSD

43
Q

Class 4 anti-arrhythmic mechanism

A

Ca channel blockers –> decreased conduction velocity

44
Q

S1 is

A

the mitral valve closing

45
Q

Class 3 anti-arrhythmics

A

AIDS: amiodarone, ibutilide, dofetilide, sotalol

46
Q

Right common and anterior cardinal vein becomes

A

SVC

47
Q

Lithium exposure in utero causes

A

Ebstein anomaly: tricuspid valve is displaced down into RV

48
Q

Things that decrease contractility

A

B1 blockade, HF with systolic dysfunction, acidosis, hypoxia, Ca channel blockers

49
Q

Rhythm control in Torsades

A

Mg

50
Q

Persistent truncus arteriosus

A

TA doesn’t divide into pulmonary trunk and aorta

51
Q

Causes of aortic regurgitation

A

BEAR: Bicuspid valve, endocarditis, aortic root dilation, rheumatic fever

52
Q

TAPVR

A

Pulmonary vein enters right heart, associated with ASD and PDA

53
Q

Causes of aortic stenosis

A

age related calcification, or calcification of bicuspid aortic valve

54
Q

Transposition of the great vessels

A

Not compatible with life without a shunt (circulations are separate)

55
Q

Dressler syndrome

A

occurs several weeks post MI, autoimmune process resulting in fibrinous pericarditis

56
Q

Pathology 0-24 hrs post MI

A

Wavy fibers or no change (0-4 hrs), early coag negrosis (4-24 hrs)

57
Q

Digoxin antidote

A

slowly normalize K, cardiac pacer, anti-dig Ab fragments, Mg

58
Q

Flow is proportional to

A

r^4

59
Q

Congenital long QT syndromes

A

loss of K channel function

60
Q

Which Ca channel blockers are cardioselective (nondihydropyrdines)

A

diltiazem and verapamil

61
Q

Hypertrophic cardiomyopathy leads to

A

diastolic dysfunction

62
Q

tachyphylactic means

A

there is an acute decrease in response to a drug after initial/repeated administration

63
Q

treatment for htn with asthma

A

ARBs, Ca channel blockers, thiazides, cardioselective beta blockers

64
Q

PDA is maintained by

A

PGE and low O2 tension

65
Q

Mycoardial action potential channels per phase

A

0: Na
1: Na is inactivated, K opens
2: Ca influx balances K efflux
3: Massive K efflux via delayed rectifying channels
4: High K permeability maintains resting potential

66
Q

4th aortic arch becomes

A

aortic arch, and proximal subclavian

67
Q

Tricuspid atresia requires

A

ASD and VSD for viability

68
Q

Class 1 anti-arrhythmic mechanism

A

Na channel blockers –> decrease slope of phase 0

69
Q

Truncus arteriosus becomes

A

ascending aorta and pulmonary trunk

70
Q

Umbilical vein becomes

A

Ligamentum teres

71
Q

coronary blood flow to LV and septum peaks in

A

early diastole

72
Q

Drugs that decrease HF mortality

A

ACE-Is or ARBs, beta blockers (not acute though), and spironolactone

73
Q

holosystolic high pitched, “blowing murmur”

A

Mitral/tricuspid regurgitation (mitral also radiates to axilla

74
Q

physiological S2 splitting is due to

A

delayed pulmonic valve closure (b/c of increased venous return on inspiration)

75
Q

Class 2 anti-arrhythmic mechanism

A

beta blockers –> decrease SA and AV node via decreased cAMP and Ca

76
Q

treatment for hypertension with HF

A

Thiazide diuretics, ACE-i/ARBs, beta blockers (compensated), aldosterone antagonists

77
Q

Most common congenital cardiac anomaly

A

Ventricular septal defect

78
Q

treatment for beta blocker overdose

A

saline, atropine, glucagon

79
Q

in 1st order kinetics, half life =

A

0.7 x Vd / Cl

80
Q

Class IB anti-arrhythmics

A

Lidocaine, phenytoin, mexiletine

81
Q

Wide S2 splitting is seen in

A

conditions that delay RV emptying (pulmonary stenosis, and right bundle branch block)

82
Q

Class 2 anti-arrhythmics (beta blockers)

A

metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

83
Q

Brugada syndrome

A

AD loss of function in Na channels –> ICD to prevent SCD

84
Q

Medication to close a patent ductus arteriosus

A

Indomethacin

85
Q

Hydralazine acts via

A

increased cGMP –> afterload reduction

86
Q

Bacterial endocarditis presentation

A

FROM JANE: Fever, Roth Spots, Osler Nodes, Murmur, Janeway lesions. Anemia, Nail-bed hemorrhage, Emboli

87
Q

holosystolic, harsh sounding murmur, loudest at tricuspid

A

Ventricular septal defect

88
Q

Treatment of hypertrophic cardiomyopathy

A

stop high intensity workouts, beta-blockers or verapamil, avoid decreasing preload.

89
Q

Use of class 2 anti-arrhythmic

A

SVT, rate control for a fib/flutter

90
Q

Pericarditis causes referred pain to

A

neck, arms, or shoulders

91
Q

treatment for htn in pregnancy

A

New Moms Love Hugs: Nifedipine, methyldopa, labetelol, hydralazine

92
Q

JONES criteria for Rheumatic heard disease

A

Joints, heart, Nodules, Erythema marginatum, Sydenham chorea

93
Q

S2 is

A

the aortic valve closing

94
Q

Congenital right to left shunts

A

5 T’s: Truncus arteriosus, transposition, tricuspid atresia, tetralogy of fallot, TAPVR

95
Q

1st aortic arch becomes

A

Maxillary artery

96
Q

Treatment of type A aortic dissection

A

surgery (ascending aorta is involved in A)

97
Q

Treatment of type B aortic dissecttion

A

Beta blockers for type B, then vasodilators (di-later-s)

98
Q

Dilated cardiomyopathy leads to

A

systolic dysfunction

99
Q

Wolff-Parkinson-White syndrome

A

most common ventricular pre-excitation syndrome, may cause SVT. Abnormal conduction bypasses AV node –> early ventricular depolarization (delta wave) –> wide QRS.

100
Q

What type of muscle has Ca induced Ca release

A

Cardiac

101
Q

Posterior, subcardinal, and supracardinal veins become

A

IVC

102
Q

Treatment of dilated cardiomyopathy

A

Na restriction, ACE-I, spironolactone, digoxin

First Aid Stuff I Don't Know (10 decks)

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