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Cardiovascular FA > MTB and important from FA > Flashcards

MTB and important from FA Flashcards

1
Q

Left circumflex coronary artery (LCX) supplies

A

Lateral and posterior walls of left ventricle

Anterolateral papillary muscle

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2
Q

Left anterior descending artery (LAD) supplies

A

Anterior 2/3 of interventricular septum
Anterolateral papillary muscle
Anterior surface of left ventricle

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3
Q

Posterior descending/interventricular artery (PDA) supplies

A

Posterior 1/3 of interventricular septum
Posterior walls of ventricles
Posteromedial papillary muscle

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4
Q

Increased pulse pressure in

A
  1. Hyperthyroidism
  2. Aortic regurgitation
  3. Aortic stiffening (isolated systolic hypertension in elderly)
  4. Obstructive sleep apnea (sympathetic tone)
  5. Exercise (transient)
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5
Q
  1. aortic arch receptors transmit via…to…

2. carotid receptors transmit via

A
  1. VAGUS 2. GLOSSOPHARYNGEAL

both to SOLITARY nucleus of medulla

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6
Q

Cushing reaction triad

A
  1. hypetension
  2. bradycardia
  3. respiratory depresion
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7
Q

Electrolyte disturbances - ECG?

A
  1. U waves and flattened T waves in low K+
  2. wide QRS and peaked T waves in high K+
  3. torsades de pointes in low Mg2+
  4. QT prolongation in low Ca2+
  5. Bradycardia/cardiac arrest in high Mg2+
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8
Q

JVP - phases

A

a wave - c wave - x descent - v wave - y descent

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9
Q

JVP - a wave

A

atrial contraction

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10
Q

JVP - c wave

A

RV contraction (closed tricuspid valve bulging atrium)

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11
Q

JVP - x descent

A

atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction

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12
Q

JVP - v wave

A

increased right pressure due to filling against closed tricuspid valve

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13
Q

JVP - y descent

A

RA emptying into RV

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14
Q

AV block 1st degree - ECG / treatment

A

The PR interval is prolonged (>200msec)

  • asymptomatic: no treatment (no matter how low HR)
  • symptomatic: atropine as initial, pacemaker as most effective
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15
Q

AV block 2nd degree - types

A

Mobitz type I (Wenckebach)

Mobitz type II

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16
Q

Mobitz 1 - ECG, treatment, causes

A

progressively lengthening PR interval that results in a dropped beat
sign of normal aging of the conduction system
treat like sinus bradycardia

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17
Q

Mobitz 2 - ECG, mechanism, treatment

A

Mobitz 2 is a far more pathologic than Mobitz 1. It just drops a brat without the progressive legthening of the PR interval. It progress or deteriorates into 3rd degree AV block. Treat like 3rd degree AV block. Everyone with Mobitz II block gets a pacemaker even if they are asymptomatic

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18
Q

3rd degree AV block

A

the atria and ventricles beat intependently of each other

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19
Q

Sinus bradycardia - treatment

A
  1. no treatment if asymptomatic (no matter how low the heart is
  2. if symptomatic: use atropine as the best initial therapy, and pacemaker as the most effective therapy
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20
Q

58 woman 2 days after MI has VT even under aspirin, heparin, lisinopril nad metoprol. next step in

A

angiography for angioplasty or bypass

manage arrhythmias from ischemia by correcting ischemia

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21
Q

when to do precordial thump?

A

very recent of onset of arrest (less than 10 minutes) with no defibrillator available (you know it is recent because you saw it hapen)

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22
Q

VT manegment

A

based on the hemodynamic status

  1. pulselss: like VF
  2. hemodynamically stable: medications (amiodarone then lidocaine then procainamide), if fail, cardiovert the patient
  3. hemodynamicallyun stable: electrical cardioversion several times, followed by medications (such as amiodarone, lidocaine or procainamide)
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23
Q

VT with hemodynamic instability is defined as

A
  1. chest pain
  2. dyspnea/CHF
  3. hypotension
  4. confusion
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24
Q

Pulseless electrical activity - treatment

A

correct the underlying cause:

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25
Q

acute AF - treatment

A
  1. hemodynamically unstable: synchronized cardioversion.
  2. hemodynamically stable: rate control (target 60-100) with b-blockers or CA2+ blokcers. After rate control is achieved, cardiovestion. Electrical cardiovesion is preferred over pharmacological (if fails or not feasible: amiodarone etc)
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26
Q

chronic atrial fibrillation - routine cardioversion

A

not indicated because the majority of these who are converted into sinus rhythm will not stay in sinus. atrial fibrillation and flutter are caused by anatomic abnormalities of the atria due to hypertension or valvural disease. Shocking into sinus rhythm does not correct a dilated LA. over 90% will revert fibrillation even with the use of of antiarrhythmic medication

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27
Q

chronic atrial fibrillation - treatment

A

the best initial therapy for fibrillation and flutter is to control the rate with beta blockers calcium channel blockers or digoxin. Once the rate is 60-100, the most appropriate next step is to give warfarin (or dabigatran, or rivaroxaban or apixaban, OR ASPIRIN IN LOW RISK).
cardioversion after 3 weeks, and then 4 weeks anticoagulation.

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28
Q

chronic atrial fibrillation - anticoagulation?

A

without: 6 embolic strokes per year for 100 patients (6%).
with: INR 2-3, the rate is 2-3%.
you need to use heparin only if there is a current clot in the atrium

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29
Q

CHADS score AND explain

A 
C: CHF score or cardiomyopathy (1)
H: hypertension (1)
A: age more than 75 (1)
D: Diabetes (1)
S: stroke or TIA (2)
when is 1 or less use aspirin
when 2 or more, use warfarin, dabigatram rivaroxaban, or apixaban
30
Q

supraventricular tachycardia - treatment

A
  1. vagal maneuvers (eg. carotid massage, Valsava, dive reflex, ice immersion)
  2. adenosine if vagal maneuvers don’t work
  3. beta blockers (metoprolol, cancium channel blockers (dilitazem), or digoxin, if adenosine is not effective
31
Q

Vagal maneuvers on SVT and on atrial fibrillation

A
  1. slow and convert SVT

2. do not convert arial fibrillation

32
Q

the most accurate test for WPW is

A

cardiac electrophysiology studies

33
Q

WPW syndrome - treatment

A
  1. acute therapy: procainamide or amiodarone for both atrial or ventricular rythm disturbances. Use them only is WPW is CURRENTLY presenting with an arrhythmia
  2. Radiofrequency catheter ablation is curative
  3. digoxin and calcium channel blokcers are dangerous in WPW. They block the normal AV node and force codunction into the abnormal pathway.
34
Q

Multifocal atrial tachycardia (MAT) is associated with / ECG

A
  • chronic lung disease such as COPD

- MAT has at least 3 different P wave morphologies

35
Q

Multifocal atrial tachycardia (MAT) - treatment

A
  • treat the underlying lung disease

- treat MAT as you would atrial fibrillation, but avoid beta blockers (because of lung diseease

36
Q

Brugada syndrome mode of inheritance / mc in / ecg

A

AD, asian male

pseudo-right bundle branch block and ST elevations in V1-3

37
Q

Brugada syndrome - management

A

ventricular tachyarrhytmias and Sudden Cardiac Death (SCD)

38
Q

torsades de pointes - caused by

A
  1. drugs
  2. decreased K+
  3. decreased Mg2+
  4. congenital abnormalities
39
Q

Congenital long QT syndrome includes (and characteristics)

A
  1. Romano-ward syndrome (AD, pure cardiac phenotype)

2. Jervell and Lange-Nielsen syndrome ( AR, sensoreneural deafness)

40
Q

drug-induced long QT

A

Mnemonic ABCDE

  1. antiArrhythmics (class IA,III)
  2. antiBiotics (eg macrolides, quinolones)
  3. antiCycchotics (eg haloperidol)
  4. antiDepressants (eg TCAs)
  5. AntiEmetics (eg ondasetron)
41
Q

MCC of secondary hypertension

A

renal/renovascular disease (eg fibromascular dysplasia found in younger women) and 1ry hyperaldosterinism

42
Q

hypertensive urgency

A

severe (>=180,120) hypertension without acute end ogran damage

43
Q

hypertensive emergency

A

severe hypertension with evidence of acute end organ damage

44
Q

hypertension left untreated: patients die from (and propotions)

A
  1. CAD or CHF (50%)
  2. stroke (33%)
  3. renal failure (10-15%)
45
Q

hypertensive emergencies drugs

A
  1. clevidipine 2. fenoldopam 3. labetolol

4. nicardipine 5.nitroprusside

46
Q

nitroprusside toxicity

A 
cyanide toxicity (releases cyanide)
(especially in high doses, prolonged infusion, hepatic or renal impairment)
47
Q

nitroprusside mechanism of action

A

increases cGMP via direct release of NO

48
Q

fenoldopam toxicity

A

. hypotension

  1. natriuresis
  2. tachycardia
49
Q

fenoldopam mechanism of action

A

dopamine D1 receptor antagonist –> coronary, peripheral, renal and splanchnic vasodilation

50
Q

fenoldopam clinical use

A
  1. hypertensive emergency

2. postoperative hypertension

51
Q

nitrates toxicity

A
  1. reflex tachycardia (treat with beta blocker)
  2. hypotension 3. flushing 4. headache
  3. Monday disease in environmental exposure
52
Q

drugs that causes hypertension

A
  1. NSAID 2. Steroids 3. alcohol 4. cocaine 5. oran contraceptives 6. nasal decongestants 7. cyclosporine
53
Q

primary essential hypertension therapy - drugs

A
  1. thiazide diuretics 2. ACE inhibitors 3. angiotensin II receptor blockers 4. dihydropyridine Ca2+ channel blockers
54
Q

hypertension with heart failure - therapy

A
  1. diuretics 2. ACE inhibitors 3. angiotensin II receptor blockers 4. β - blockers (compensated HF) 5. Aldosterone antagonist
55
Q

hypertension in pregnancy - drugs and short mechanism of action

A
  1. hydralazine (vasodilator by cGMP increasing)
  2. labetolol (alpha-beta blocker)
  3. methyldopa (a-2 blocker)
  4. nifedipine (dihydropiridine Ca2+ channel blocker)
56
Q

Hypertension with diabetes mellitus -therapy (drugs)

A
  1. ACE inhibitors
  2. angiotensin II receptor blockers
  3. thiazide diuretics
  4. β - blockers
57
Q

Hydralazine toxicity

A
  1. compensatory tachycardia (contraindicated in angina/CAD)
  2. LUPUS - LIKE SYNDROME
  3. Fluid retention 4. Headache
  4. Angina
58
Q

dihydropyridines vs non-dihydropyridines (side of action)

A
  1. didydropyridines –> act on vascular SMCs

2. non-dihydropyridines –> act on heart

59
Q

non - dihydropiridines - drugs

A
  1. diltiazem

2. verapamil

60
Q

dihydropyridines - drugs

A

-DIPINE

amlodipine, clevidipine, nicardipine, NIFEDIPINE, nimodipine

61
Q

diltiazem vs verapamil according to action on vscular SMCs

A

diltiazem is more effective

62
Q

calcium channel blockers - clinical uses - dihydropyridines

A
  1. hypertension (except nimodipine)
  2. angina (including printzmetal) (except nimodipine)
  3. Raynaud (except nimodipine)
  4. subarachnoid hemorrhage (only nimodipine)
  5. hypertensive urgency or emergency (only clevidipine)
63
Q

digoxin clinical use

A
  1. HF (increases contractility)

2. atrial fibrillation (decreases conduction at AV nobe and depression of SA node - via vagus)

64
Q

digoxin antidote

A
  1. slowly normalize K+
  2. cardiac pacer
  3. Mg2+
  4. anti-digoxin Fab fragments
65
Q

Digoxin toxicity

A
  1. Cholinergic (nausea, vomiting diarrhea, BLURRY YELLOW VISION, arrhytmias, AV block
  2. Hyperkalemia (poor prognosis)
66
Q

Factors predisposing digoxin toxicity

A
  1. Renal failure (decreased excretion),
  2. hypokalemia (permissive for Digoxin binding at K+ binding site on ATPase
  3. Drugs - amiodarone, verapamil, quinidine (decreased digoxin clearance, displace digoxin from tissue binding sites)
67
Q

Ranolazine - clinical use

A

angina refractory to other medical therapies

68
Q

Ranolazine - adverse effects

A
  1. constipation
  2. dizziness
  3. headache
  4. nausea
  5. QT prolongation
69
Q

dihydropyridine - side effects

A
  1. peripheral edema
  2. flashing
  3. dizziness
  4. gingival hyperplasia
70
Q

Non-dihydropyridine - side effects

A
  1. cardiac depression
  2. AV block
  3. Hyperprolactinemia
  4. constipation

Cardiovascular FA (8 decks)

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