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Cardiology > CV > Flashcards

CV Flashcards

1
Q

Antiarrhythmics

A 
No Bad boy Keeps Clean in the AM:
Class I: Na+ channel blockers
Class II: Beta blockers
Class III: K+ channel blockers
Class IV: Ca2+ channel blockers
Other: Adenosine, Mg2+
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2
Q

Class I Antiarrhythmics

A

Na+ Channel Blockers: Decrease slope of Phase 0, increase AP threshold
Class IA: Double Quarter Pounder- Disopyramide, Quinidine, Procainamide
Class IB: Lettuce, Tomato, Mayo- Lidocaine, Tocainide, Mexiletine
Class IC: Fries Please- Flecainide, Propafenone

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3
Q

Na+ Channel Blockers

A

Class I Antiarrhythmics
Class IA: Double Quarter Pounder- Disopyramide, Quinidine, Procainamide
Class IB: Lettuce, Tomato, Mayo- Lidocaine, Tocainide, Mexiletine
Class IC: Fries Please- Flecainide, Propafenone

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4
Q

Disopyramide

A

Class 1A Antiarrhythmic (Na+ channel blocker): Double Quarter Pounder- Disopyramide, Quinidine, Procainamide
*Class 1As prolong AP

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5
Q

Quinidine

A

Class 1A Antiarrhythmic (Na+ channel blocker): Double Quarter Pounder- Disopyramide, Quinidine, Procainamide

  • Class 1As prolong AP
  • Quinidine can cause cinchonism (headache, tinnitus), thrombocytopenia, torsades de pointes d/t prolonged QT
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6
Q

Procainamide

A

Class 1A Antiarrhythmic (Na+ channel blocker): Double Quarter Pounder- Disopyramide, Quinidine, Procainamide

  • Class 1As prolong AP
  • Procainamide is used for WPW, and can cause drug-induced SLE with antihistone ab (SHIPP cause drug-induced SLE)
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7
Q

Antiarrhythmic that can cause cinchonism, thrombocytopenia, torsades de pointes

A

Quinidine (Class 1A)

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8
Q

Antiarrhythmic used for WPW that can cause drug-induced SLE

A

Procainamide (Class 1A)

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9
Q

Lidocaine

A

Class 1B Antiarrhythmic (Na+ channel blocker): Lettuce, Tomato, Mayo- Lidocaine, Tocainimide, Mexiletine
*Class 1Bs shorten AP; preferentially affect ischemic/depolarized tissue; useful in acute post-MI v.tach and digitalis-induced arrhythmias

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10
Q

Mexiletine

A

Class 1B Antiarrhythmic (Na+ channel blocker): Lettuce, Tomato, Mayo- Lidocaine, Tocainimide, Mexiletine
*Class 1Bs shorten AP; preferentially affect ischemic/depolarized tissue; useful in acute post-MI v.tach and digitalis-induced arrhythmias

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11
Q

Tocainide

A

Class 1B Antiarrhythmic (Na+ channel blocker): Lettuce, Tomato, Mayo- Lidocaine, Tocainimide, Mexiletine
*Class 1Bs shorten AP; preferentially affect ischemic/depolarized tissue; useful in acute post-MI v.tach and digitalis-induced arrhythmias

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12
Q

Antiarrhythmic that shortens AP; preferentially affects ischemic/depolarized tissue; useful in acute post-MI v.tach and digitalis-induced arrhythmias

A

Class 1Bs: Lettuce, Tomato, Mayo- Lidocaine, Tocainimide, Mexiletine

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13
Q

Flecainide

A

Class 1C Antiarrhythmic (Na+ channel blocker): Fries Please- Flecainide, Propafenone

  • Class 1Cs have no effect on AP duration; last resort in refractory tachyarrhythmias
  • IC is Contraindicated in structural heart disease and post-MI
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14
Q

Propafenone

A

Class 1C Antiarrhythmic (Na+ channel blocker): Fries Please- Flecainide, Propafenone

  • Class 1Cs have no effect on AP duration; last resort in refractory tachyarrhythmias
  • IC is Contraindicated in structural heart disease and post-MI
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15
Q

Antiarrhythmics that are contraindicated in structural heart disease and have no effect on AP duration and are last resort in refractory arrhythmias

A

Class 1C: Fries Please- Flecainide, Propafenone

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16
Q

Class II Antiarrhythmics

A

Beta-blockers (no Bad boy keeps clean in AM): METAP- Metoprolol, Esmolol, Timolol, Atenolol, Propranolol

  • Beta-blockers decrease nodal activity by decreasing cAMP, decreasing Ca2+ currents, decreasing Phase 4 slope (nodal)
  • Beta-blockers used for v.tach, SVT, A.fib/flutter
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17
Q

Beta blockers in arrhythmia

A

Class II Antiarrhythmics: decrease nodal activity by decreasing cAMP, decreasing Ca2+ current, decreasing Phase 4 slope
*Beta-blockers used for v.tach, SVT, A.fib/flutter

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18
Q

Metorpolol in antiarrhythmia

A

Class II Antiarrhythmics: decrease nodal activity by decreasing cAMP, decreasing Ca2+ current, decreasing Phase 4 slope

  • Beta-blockers used for v.tach, SVT, A.fib/flutter
  • Metoprolol can cause dyslipidemia (tx OD with glucagon)
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19
Q

Propranolol in antiarrhythmia

A

Class II Antiarrhythmics: decrease nodal activity by decreasing cAMP, decreasing Ca2+ current, decreasing Phase 4 slope

  • Beta-blockers used for v.tach, SVT, A.fib/flutter
  • Propranolol can exacerbate vasospasm in Prinzmetal’s angine
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20
Q

Class III Antiarrhythmics

A

K+ Channel Blockers (no bad boy Keeps clean): AIDS- Amiodarone, Ibutilide, Dofetilide, Sotalol
*Class III works on Phase 3: prolongs AP, prolongs ERP, prolongs QT interval

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21
Q

K+ channel blockers

A

Class III antiarrhythmics (no bad boy Keeps clean): AIDS- Amiodarone, Ibutilide, Dofetilide, Sotalol
*Class III works on Phase 3: prolongs AP, prolongs ERP, prolongs QT interval

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22
Q

Amiodarone

A

Class III antiarrhythmic K+ channel blocker: prolongs AP, ERP, QT interval

  • Amiodarone tox: pulmonary fibrosis, hepatotox, hypo/hyperThyroidism, corneal deposits, blue/gray skin deposits causing photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF
  • Has class I, II, III effects bc alters lipid membrane
  • Check PFTs, LFTs, TFTs!!!
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23
Q

Antiarrhythmic that causes lung, liver, thyroid disease; can also cause photodermatitis; heart problems

A

Amiodarone (class III, K+ channel blocker):

  • Used for WPW
  • Amiodarone tox: pulmonary fibrosis, hepatotox, hypo/hyperThyroidism, corneal deposits, blue/gray skin deposits causing photodermatitis, neurologic effects, constipation, bradycardia, heart block, CHF
  • Has class I, II, III effects bc alters lipid membrane
  • Check PFTs, LFTs, TFTs!!!
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24
Q

Drugs that cause photosensitivity

A

SAT: Sulfonamides, Amiodarone, Tetracyclines

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25
Q

Sotalol

A 
Class III (K+ channel blocker): prolongs AP, ERP, QT interval
*Sotalol tox: torsades de pointes (same with Ibutilide), excessive Beta block
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26
Q

WPW drugs

A

Procainamide (Class 1A, Na+ channel blocker, “pounder”) and Amiodarone (Class III, K+ channel blocker)

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27
Q

MI Evolution on Light Microscopy

A

0-4 hrs: Minimal change

4-12 hrs: Early coagulative necrosis, edema, hemorrhage, wavy fibers

12-24 hrs: Coagulation necrosis & marginal contraction band necrosis (from reperfusion injury); Grossly dark mottling tissue (pale on tetrazolium stain)

1-5 days: Coagulation necrosis and neutrophilic infiltrate; Grossly hyperemia

5-10 days: Macrophage phagocytosis of dead cells; Grossly yellow-brown softening with hyperemic border

10-14 days: Granulation tissue & neovascularization; Grossly yellow -> white?

2 weeks-2 months: Collagen deposition and scar formation; Grossly white?

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28
Q

MI 0-4hr

A

Minimal change; Risk of arrhythmia, CHF exacerbation, shock

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29
Q

MI 4-12hr

A

Troponins begin to rise (up to 7-10 days), early coagulative necrosis with edema, hemorrhage, wavy fibers; Risk of arrhythmia

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30
Q

MI 12-24hr

A

Coagulation necrosis & marginal contraction band necrosis (from reperfusion injury); Grossly dark mottling tissue (pale on tetrazolium stain); Risk of arrhythmia

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31
Q

MI 1-5 days

A

Coagulation necrosis and neutrophiling infiltrate; Grossly hyperemia; Risk of fibrinous pericarditis

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32
Q

MI 10-14 days

A

Granulation tissue (macrophages phagocytosing cells) & neovascularization; Grossly yellow -> white? Risk of tamponade, papillary rupture, ventricular aneurysm, interventricular septal rupture d/t macrophages degrading wall

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33
Q

MI 2 weeks-2 months

A

Collagen (type 1) deposition and scar formation; Grossly gray-white muscle with recanalized artery; Risk of Dressler’s syndrome

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34
Q

Post-MI Cx: Arrhythmia

A

First few days

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35
Q

First few days Post-MI Cx

A

Arrhythmias, LV failure, pulmonary edema, cardiogenic shock, fibrinous pericarditis (1-3d)

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36
Q

Post-MI Cx: LV failure, pulmonary edema, cardiogenic shock

A

First few days

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37
Q

Post-MI Cx: Fibrinous pericarditis

A

1-3 days; Dressler’s syndrome 2 weeks+

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38
Q

Post-MI Cx: Ventricular free wall rupture

A

3-14 days

Leads to tamponade

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39
Q

Post-MI Cx: Papillary muscle rupture

A

3-14 days

Leads to severe mitral regurgitation

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40
Q

Mitral Regurgitation in Post-MI patient

A

Papillary muscle rupture

Usually occurs 3-14 days after MI

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41
Q

Post-MI Cx: Interventricular septum rupture

A

3-14 days

Leads to VSD

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42
Q

Post-MI Cx: Ventricular aneurysm formation

A

3-14 days (esp 1 week)

Decreased CO, risk of arrhythmia -> thrombus

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43
Q

3-14 days Post-MI Cx

A

Ventricular free wall rupture -> tamponade; Papillary muscle rupture -> mitral regurg; Interventricular septum rupture -> VSD; Ventricular aneurysm formation -> embolus

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44
Q

1-3 days Post-MI Cx

A

Fibrinous pericarditis- friction rub

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45
Q

2 weeks+ Post-MI Cx

A

Dressler’s syndrome: autoimmune fibrinous pericarditis

46
Q

MI with ECG changes in V1-V4

A

Anterior Wall (LAD)

47
Q

MI with ECG changes in V1-V2

A

Anteroseptal Wall (LAD)

48
Q

MI with ECG changes in V4-V6

A

Anterolateral Wall (LCX)

49
Q

MI with ECG changes in I, aVL

A

Lateral Wall (LCX)

50
Q

MI with ECG changes in II, III, aVF

A

Inferior Wall (RCA)

51
Q

STEMI

A

Transmural infarct

52
Q

ST-depression MI

A

Subendothelial infarct

53
Q

Progression of ECG changes in Transmural MI

A

ST elevation (acute) -> Q wave appears (hours) -> T way inversion (1-2 days)

  • ST normalizes days later
  • Q wave remains
  • T wave normalizes weeks later
54
Q

Blood supply of SA and AV nodes

A

RCA. RCA occluseion -> arrhythmia

55
Q

Posterior descending artery

A

85% is Right-dominant (arises from RCA)

Rest are either off LCX or both

56
Q

Most posterior part of heart

A

LA. Enlargement -> dysphagia, hoarseness

57
Q

CO

A

CO = SV x HR = Rate of O2 Consumption / (Art O2 Content - Ven O2 Content) = MAP / TPR

58
Q

MAP

A

MAP = CO x TPR (P=QR Ohm’s Law) = 2/3 DBP + 1/3 SBP

  • Total R in series = Sum
  • Total 1/R in parallel = Sum of 1/R’s
59
Q

Pulse Pressure

A

PP = SBP - DBP = proportional to SV

Widened in Aortic Regurgitation

60
Q

EF

A

EDV - ESV / EDV

Normally ≥55%

61
Q

CO in exercise

A

CO maintained at first by increasing SV and HR, but SV plateaus -> later maintained by increasing HR. If HR too high, diastolic filling of coronary arteries is incomplete.

62
Q

SV is affected by what?

A

SV CAP: Contractility, Afterload, Preload

*SV is increased in anxiety (CA), exercise (preload and CA), pregnancy (preload)

63
Q

Contractility is affected by what?

A
  • Increased by Catecholamines (bind B1 receptor -> increase Ca pump activity in SR), Ca2+, decreased Na+, Digoxin
  • Decreased by Beta1 blockade (decrease cAMP), heart failure, acidosis, hypoxia/hypercapnia, Verapamil and Diltiazem (non-dihydropyridine CCBs)
64
Q

Preload and Afterload are determined by what?

A
  • Preload: blood volume, exercise (slightly), excitement. vEnodilators decrease prEload.
  • Afterload: MAP, TPR. vAsodilators decrease Afterload.
  • ACE-I/ARBs decrease both preload and afterload
65
Q

Starling Curve

A

CO or SV v. EDV (preload):

  • Increased curve with exercise, CA, contractility
  • Decreased curve with CHF (but is hyperbole- there is a “sweet spot” of fluid volume status), improved by digoxin
  • *Starling Curve demonstrates how the force of contraction is proportional to the preload (preload affects force but not contractility)
66
Q

Viscosity of Blood

A

Resistance (P=QR -> R=P/Q=8(nu)(viscosity)(length)/(pi*r^4)). In other words, viscosity (hematocrit) affects the resistance to flow.

  • Viscosity increased in Polycythemia, Hyperprotein states (MM), Hereditary Spherocytosis.
  • Viscosity decreased in anemia
67
Q

Resistance to flow

A

Increased by viscosity and vessel length

Decreased by radius to the 4th power

68
Q

Radius of vessel and resistance

A

Increased radius -> decreased resistance by radius to the 4th power

69
Q

AV shunt

A

decreases TPR, increasing SV for given contractility and preload

70
Q

Dicrotic notch

A

On aortic pressure curve, is jump in pressure when aortic valve closes, due to elasticity of aorta.

  • Important for coronary bloodflow
  • Decreased elasticity seen in Syphyllis and Marfan’s
71
Q

JVP curve

A

“at carter’s x-ing, vehicles yield”

a: R atrial contraction
c: R ventricular contraction
x: descent of tricuspid valve during ventricular contraction and atrial relaxation
v: R atrial filling
y: blood flows from RA to RV

72
Q

S1

A

mitral and tricuspid valves close, loudest at mitral area

73
Q

S2

A

aortic and pulmonic valves close, loudest at left sternal border

74
Q

S3

A
  • Rapid Ventricular Filling in mitral regurgitation, CHF, dilated ventricles, L->R shunt
  • Normal in children and pregnant women
75
Q

S4

A

*Atrial kick against stiff LV in LVH, AS, post-MI

76
Q

S2 splitting

A

Normal: Inspiration causes drop in intrathoracic presure and increased RV return -> delayed closing of pulmonic valve
Wide: Delayed RV emptying in pulmonic stenosis, RBBB
Fixed: Increased R volumes in ASD (L->R shunt)
Paradoxical: Delayed LV emptying in aortic stenosis, LBBB

77
Q

Wide S2 splitting

A

Delayed RV emptying: Pulmonic Stenosis, RBBB

78
Q

Fixed S2 splitting

A

Increased flow through pulmonic valve d/t increased RA and RV volumes, always delayed: ASD (L->R shunt)

79
Q

Paradoxical S2 splitting

A

Delayed LV emptying, so that on inspiration, P2 moves closer to A2: Aortic Stenosis, LBBB

80
Q

Holosystolic murmur loudest at apex, radiating to axilla

A

MR d/t ischemic heart disease, MVP, LV dilation, rheumatic fever, infective endocarditis

81
Q

Holosystolic murmur loudest at LLSB, radiating to RSB

A

TR d/t RV dilation, rheumatic fever, infective endocarditis

82
Q

Heart sounds heard best in LLD position

A

Mitral stenosis, mitral regurgitation, S3, S4

83
Q

Systolic murmur following ejection click, radiating to carotids

A

Aortic Stenosis (crescendo-decrescendo) d/t age-related calcification (>60), congenital bicuscpid (>40), chronic rheumatic valve dz, unicuspid valve, syphillis

  • Ejection click is due to abrupt halting of valve leaflets
  • Pulsus parvus et tardus: weak, delayed upstroke pulse
  • Cx: SAD (syncope, angina, dyspnea)
84
Q

Holosystolic murmur heard best at tricuspid area, accentuated with hand grip maneuver

A

VSD: Hard to distinguish from TR

*Hand grip increases afterload

85
Q

Late systolic murmur with midsystolic click enhanced by standing or valsalva

A

MVP best hear over apex: click due to sudden tensing of chordae tendinae

  • Can be d/t myxomatous degeneration, rheumatic fever, chordae rupture
  • Standing and valsalva decrease venous return
  • Risk of endocarditis ONLY if also mitral regurg (need endothelial damage by turbulent blood flow)
86
Q

Diastolic decrescendo murmur with wide pulse pressure, enhanced with hand grip

A

AR +/- head bobbing and bounding pulses

  • Often d/t aortic root dilation (Syphillis, Marfan’s), bicuspid aortic valve, endocarditis, rheumatic fever
  • Hand grip increases afterload
  • Vasodilators decrease murmur intensity
87
Q

Late diastolic murmur following opening snap, enhanced by expiration

A

MS: OS is mitral leaflets halting after rapid opening from being fused. LA&raquo_space; LV during diastole

  • D/t rheumatic fever
  • Can result in LA dilation
  • Expiration increases LA return (Split S2 is exacerbated by inspiration, while this opening snap is exacerbated by expiration)
88
Q

Continuous machine-like murmur, loudest at S2

A

PDA d/t rubella or prematurity

89
Q

Normal heart sounds in absence of symptoms

A

Split S1, Split S2 on inspiration, S3 in patient under 40, Early quiet systolic murmur

90
Q

Speed of conduction of cardiac cells

A

PAt VAV: Purkinje fastest > Atria > Ventricles > AV node

91
Q

PR interval >200 ms

A

200ms=1 large box

Primary heart block

92
Q

QRS complex duration

A

120ms = 3 small boxes

If longer = ventricular rhythm

93
Q

T wave and potassium

A

T wave inversion suggests low K+ and may indicate recent MI

94
Q

ST segment

A

isoelectric (ventricles depolarized)

95
Q

U wave

A

hypoK+ and bradycardia

96
Q

Small box on ECG, Big box

A

Small box = .04s

Big box = .2 s = 200ms

97
Q

Torsades de pointes

A

Ventricular tachycardia with shifting sinusoidal waveforms. Can progress to V.fib
*D/t anything that prolongs QT: Macrolides, antimalarials, haloperidol, methadone, protease inhibitors, antiarrhythmics (Class1A, Class III); or congenital long QT (Na or K channel mutation)
Tx: Magnesium Sulfate

98
Q

WPW

A

Accessory pathway bypassing AV node -> early QRS (Delta wave) -> may result in reentry current -> SVT
Tx: Procainamide or Amiodarone
*Do not give adenosine in WPW! (normally given for SVTs)

99
Q

Atrial fibrillation

A

Often d/t large atrium -> irregularly irregular, no discrete P waves -> SVT, stasis or stroke
*Tx: Less than 48 hr -> Cardioversion; Longer than 48hr -> Heparin, Warfarin, Rate/Rhythm control (Digoxin, beta blocker, CCB, Sotalol, Amiodarone)

100
Q

Atrial Flutter

A

Back to back identical atrial depolarization waves -> sawtooth
*Tx: Class IA, IC, III antiarrhythmics for rhythm; Beta blocker or CCB for rate

101
Q

Ventricular Fibrillation

A

Erratic with no identifiable waves (no sinusoidal pattern), fatal without immediate CPR/defibrillation

102
Q

Ventricular tachycardia with shifting sinusoidal waveforms

A

Torsades de pointes, can progress to V.fib
*D/t anything that prolongs QT: Macrolides, antimalarials, haloperidol, methadone, protease inhibitors, antiarrhythmics (Class1A, Class III); or congenital long QT (Na or K channel mutation)
Tx: Magnesium Sulfate

103
Q

Accessory pathway bypassing AV node -> early QRS (Delta wave)

A

WPW: may result in reentry current -> SVT
Tx: Procainamide or Amiodarone
*Do not give adenosine in WPW! (normally given for SVTs)

104
Q

Often d/t large atrium -> irregularly irregular, no discrete P waves -> SVT, stasis or stroke

A

A.fib:
*Tx: Less than 48 hr -> Cardioversion; Longer than 48hr -> Heparin, Warfarin, Rate/Rhythm control (Digoxin, beta blocker, CCB, Sotalol, Amiodarone)

105
Q

Back to back identical atrial depolarization waves -> sawtooth

A

Atrial Flutter

*Tx: Class IA, IC, III antiarrhythmics for rhythm; Beta blocker or CCB for rate

106
Q

Erratic with no identifiable waves (no sinusoidal pattern)

A

V.fib: fatal without immediate CPR/defibrillation

107
Q

What bug can cause AV block?

A

B. burgdorferi (Lyme disease) -> Can progress to Complete (3rd degree) AV block

108
Q

Progressive lengthening of the PR interval until a beat is dropped (P wave without QRS)

A

Mobitz type I 2nd degree AV block, aka Wenckebach

109
Q

2 P-waves : 1 QRS

A

Mobitz type II 2nd degree AV block, may progress to 3rd degree, treat with pacemaker

110
Q

No relationship between P-waves and QRS complexes. Atrial rate is faster than ventricular rate. But QRS waves are narrow.

A

3rd degree (Complete) AV block

Cardiology (3 decks)

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