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Professional Development > Part 17 > Flashcards

Part 17 Flashcards

1
Q

3 routine therapies for heart failure and how they impact the condition

A
  • diuretics (decrease preload, afterload, pulmonary edema, cardiac distension)
  • RAAS inhibitors (promote dilation of artereioles and veins and decrease aldosterone release)
  • B blockers (not understood mechanism)
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2
Q

DOC for patients with severe heart failure and why

A

Loop diuretics (furosemide), promote strong diuresis and work even when GFR is low

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3
Q

sacubitril/valsartan (entresto) drug class, function, and mech of action

A
  • Angiotensin receptor neprilysin inhibitor (ARNI)
  • approved for patients with class II-IV HF to be used in place of an ACEI or ARB as it is superior than elanapril alone when looking at reduced risk of CV related death
  • functionally increases natriuretic peptide levels by inhibiting neprilysin that breaks them down
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4
Q

sacubitril/valsartan (entresto) ADR’s (4)

A
  • hypotension by volume depletion
  • cough
  • hyperkalemia
  • fetal harm
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5
Q

Aliskiren (tekturna) function

A

Can shut down RAAS by binding renin, should work as well as ACEI and ARB’s but is only approved for HTN and not for treatment of HF (doesn’t improve outcomes)

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6
Q

Ivabradine (Corlanor) drug class and indications

A
  • SA node inhibitor (selective for funny channels slowing firing of SA node and reducing HR)
  • indicated for patients with resting HR of at least 70bpm and are on max doses of B blockers or have contraindications of it, and have and LVEF equal or less than 35%
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7
Q

Aldosterone antagonists functions (2) and two examples

A
  • Block receptors for aldosterone in heart and blood vessels, can prevent myocardial remodeling and delay fibrosis (aldosterone increases fibrosis of myocardium and vascular) (as well as its original function to prevent Na+ and thus H2O retention with K+ excretion)
  • spironolactone and eplerenone
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8
Q

Ivabradine (Corlanor) ADR’s (3) and contraindications (3)

A
  • Bradycardia
  • hypertension
  • afib
  • Low BP
  • sick sinus syndrome
  • 3rd degree heart block
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9
Q

Dopamine (inocor) function at diff doses

A

Low - stimulate kidneys
Intermediate - increase inotropy and thus SV/CO
Large - stimulates a1 receptors on vascular smooth muscle producing vasoconstriction

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10
Q

Nitroglycerin function

A

Potent venodilator causing a dramatic decrease in preload on the heart, in HF used to reduce acute severe pulmonary edema but should not be taken with PDE5 inhibitors such as sildenafil

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11
Q

Sodium nitroprusside (nitropress) function

A

Agent to rapidly dilate arterioles and veins for short term therapy of severe HF

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12
Q

Digoxin (lanoxin, loxicaps) mech of action

A
  • accelerates entry of Ca2+ into cardiac muscle cells
  • during AP, Na+ and Ca2+ enter cardiac muscle cells and K+ exits
  • Then Na/K ATPase pumps things back and Ca2+ leaves via Na/Ca transporter
  • Inhibits adenosine triphophate (ATPase which energizes Na+/K+ pump
  • buildup stimulates exchane of Na for Ca2+, increasing levels in cell
  • greater contraction
  • too much K+ will inhibit effect of digoxin
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13
Q

What must be monitored and kept in normal range when on digoxin?

A

K+

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14
Q

Drug for patients with bradycardia or AV block due to digoxin toxicity and why

A

Atropine - it is an anticholinergic that inhibits parasympathetic action on the heart, therefore reversing some of the effect of digoxin toxicity via a separate mechanism

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15
Q

Pericarditis signs and symptoms (3)

A
  • sharp chest pain relieved by sitting and leaning forward
  • rhythmic pericardial friction rub usually at the left lower sternal border not associated with respiratory rate
  • Retrosternal pain radiating to neck, shoulders, back
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16
Q

Pericarditis has the potential to sequellae into ____ requiring ____

A

cardiac tamponade, pericardiocentesis of fluid

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17
Q

Becks triad for acute cardiac tamponade

A
  • low arterial bp
  • increased central venous pressure
  • distant heart sounds (muffled)
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18
Q

Best diagnostic test for pericrditis and finding on that test indicating positive result

A

EKG - diffuse ST elevation across all leads except AVR (fuck AVR man it don’t do shit)

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19
Q

Chest x ray findings for pericarditis

A

“water bottle” heart (can’t tell where the pericardium ends and where the heart begins but the shape is helpful to diagnose)

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20
Q

Post MI pericarditis

A

Occurs 2-5 days*** (diff from dressler syndrome) after infarction due to inflammatory response to necrosis, will see symptoms of both post MI and pericarditis despite self resolving after period of time sometimes requiring pain management for small pericardial effusions

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21
Q

Dressler’s syndrome will have ___ pericardial effusions, and how often does it cause tamponade? When does it occur?

A

Large, rare, occurs weeks to months*** after MI or open heart surgery

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22
Q

Most common viral cause of myocarditis

A

-coxsackie virus B

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23
Q

When I say diffuse ST segment elevation you say ___. When I say nonspecific ST segment changes you say ____

A

pericarditis, myocarditis

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24
Q

Bed rest and myocarditis

A

-Not recommended to remain in bed but do not recommend exercise or exert self

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25
Q

Constrictive pericarditis

A

Thickened, fibrotic adherant pericardium due to injury (surgery) or infection that causes restricted diastolic filling

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26
Q

Infective endocarditis

A

Infection of the hearts endocardial surface, most commonly involving the valves but may also occur at a septal defect or chordae tendinae, can be acute or subacute

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27
Q

Risk factors associated with infective endocarditis (5)

A
  • underlying cardiac structural abnormalities
  • pacemaker infections
  • prolonged surgery
  • catheter related bacteremia
  • IV drug abuse or piercings
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28
Q

3 big presenting signs and symptoms of endocarditis

A
  • fever
  • onset of new murmur
  • positive blood cultures
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29
Q

Microorganisms associated with native valve endocarditis (3)

A
  • S aureus (skin, iv drug use)
  • viridans group streptococci (most common)
  • HACEK (haemophilus, actinobacillus, cardiobacterium, eikenella, kingella: uncommon, seen in immunocompromised hosts)
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30
Q

Signs of embolization of vegetation from infective endocarditis in periphery (4)

A
  • pectechiae (small hemorrhages sometimes in nailbeds [called splinter hemorrhages])
  • osler’s node (painful, purple lesions on fingers and toes)
  • janeway lesions (flat, painless red lesions on palms and soles)
  • roth spots (retinal hemorrhages with pale or yellow centers)
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31
Q

Blood culturing process for infective endocarditis

A
  • 3 sets drawn at least 1 hour apart for 3 diff mediums (aerobic, anaerobic, fungal)
  • as soon as positive is obtained then starting broad spectrum antibiotic treatment
  • narrow down once culture and sensitivity obtained
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32
Q

IV drug users will see growth of vegetation mostly on ____ sided valves

A

Right

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33
Q

Valvular dehiscence

A

Refers to the separating of an artificial valve from its anchor due to vegetation overgrowth resulting in rocking motion of prosthetic valve back and forth with blood flow

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34
Q

Infective endocarditis treatment (2)

A

Hospitalization and IV antibiotics:

  • PCN and gentamycin IV daily for 4 weeks (most common)
  • vanco or ceftriaxone IV daily 4 weeks
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35
Q

5 year mortality of infective endocarditis

A

54-87%

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36
Q

Procedures that put patients at elevated risk of infective endocarditis and which is most common? (5)

A
  • endoscopy
  • colonoscopy
  • dental extractions
  • TURP (most common)
  • transesophageal echocardiography
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37
Q

Antibiotic prophylaxis for infective endocarditis (2)

A
  • amoxicillin 2 g 1 hr prior to procedure***
    • clindamycin 600mg if allergic
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38
Q

Syncope definition

A

Transient loss of consciousness due to global cerebral hypoperfusion characterized by rapid onset, short duration, and spontaneous complete recovery (not lethargic upon return)

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39
Q

Diagnosis of syncope must rule out these 2 things

A

head trauma and epilepsy

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40
Q

Syncopal recurrence is about __%

What are the 3 types of syncope and which are favorable and which are unfavorabe?

A

20,

  • Reflex (neutrally mediated) syncope/vasovagal (favorable outcome)
  • Orthostatic hypotension (favorable outcome)
  • Untreated cardiac syncope (greater chance of mortality, unfavorable)
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41
Q

Orthostatic blood pressure measurements

A

A series of 3 measurements going from lying, sitting, to standing, if systolic BP drop greater than 20 mmHg or diastolic 10 mmHg then considered positive (or if HR increases 20-30bpm or if patient becomes symptomatic)

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42
Q

Neurally mediated (reflex) syncope/vasovagal syncope mech of action

A
  • Baroreceptors in carotid sinus and aortic arch monitor BP and HR by innervation of CN IX and X
  • Decreased firing due to lack of stretch from baroreceptors activates brain stem to respond with sympathetic innervation to raise pressure
  • Increased firing due to stretch from baroreceptors inhibits brain stem from responding with sympathetic innervation causing lowering of blood pressure as well as increase in vagal tone to heart to decrease HR
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43
Q

Carotid sinus hypersensitivity (charcot weiss baker syndrome)

A

Occurs when stimulation of carotid sinus causes bradycardia and hypotension often in elderly or with tight collars, can diagnose with carotid sinus massage

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44
Q

Orthostatic hypotension syncope etiology

A

-Sudden decrease in BP after standing or during standing after exertion due to volume depletion, drugs, or autonomic dysfunction, most common in elderly and rare in those less than 40 years of age caused by autonomic failure, drugs, hypovolemia, and treated with volume replacement, avoiding precipitating factors, treatment of underlying cause

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45
Q

Long QT syndrome and how it relates to syncope

A

Problem with heart’s electrical system that is often asymptomatic until sudden syncopal episode, may be congenital or acquired, and is linked to sudden cardiac death and torsades de pointes

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46
Q

DOC for torsades de pointes

A

-IV magnesium

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47
Q

1 treatment for long QT syndrome (and its supplement)

A
  • IV magnesium followed (stabilize) by B blocker
  • sometimes supplementary implantable cardioverter defibrillators in those with high risk for sudden cardiac death expected to live more than a year
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48
Q

Brugada syndrome

A

Genetic condition channelopathy responsible for 4-12% of all sudden cardiac deaths, high risk, manifests with specific “saddle-like” pattern ST segment elevation in leads V1-V3 and right bundle branch block

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49
Q

Brugada syndrome treatment

A

Implantable cardioverter defibrillator (ICD)

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50
Q

Wolff parkinson White syndrome

A

Frequently encountered ventricular pre-excitation syndrome, presents asymptomatic or with a paroxysmal supraventricular tachycardia or atrial fib, has triggers such as exercise or drugs, presence of delta wave on QRS complex, most have good prognosis if asymptomatic

51
Q

Wolff parkinson white treatment both urgent (3) and non-urgent (1)

A

Urgent (in afib) - syncronized direct cardioversion, if hemodynamically stable can use vagal maneuvers or iv adenosine

Nonurgent - catheter ablation

52
Q

Sick sinus syndrome and 3 subtypes

A
  • Sinus node dysfunction (normal rate and rhythm with a pause) with associated symptoms
  • 3 subtypes including chronic bradycardia, alternating sinus bradycardia with paroxysmal supraventriclar tachyarrhythmias, or tachybrady syndrome
53
Q

Peripheral arterial disease

A

Atherosclerosis of blood vessels other than the coronary or cerebral arteries leading to obstruction

54
Q

Critical limb ischemia

A

Ischemic rest pain, a non healing wound, or gangrene due to progression from claudication resulting in severe peripheral arterial disease

55
Q

The 5 P’s of acute limb ischemia that indicate severe peripheral arterial disease

A 
Pain
Pulseless
Pallor
Paresthesias
Paralysis
Poikilothermia (the rare 6th P)
56
Q

Ankle brachial index and value ranges

A
  • Division of the lower extremity systolic pressure by the brachial artery systolic pressure to determine if there is arterial disease causing claudication to the lower extremity
  • value of 1 is normal and values less than .8 indicate moderate to severe arterial disease
57
Q

Gradation of pulse intensity on physical exam

A 
0 - absent
1 - diminished
2 - normal
3 - strong
4 - bounding
58
Q

Gold standard diagnostic for evaluation of peripheral arterial disease

A

Peripheral angiography

59
Q

Peripheral venous disease presentation vs peripheral arterial disease

A
  • Venous has leg swelling and aching
    • Arterial has sharp intermittent pain
60
Q

D Dimer test for DVT

A

Elevated in nearly all patients with acute DVT so highly sensitive however picks up many false positives from any other clot formed in body, so should only be used to rule out DVT

61
Q

DVT prevention DOC

A

Low molecular weight heparin (no lab monitoring required, and has high bioavailability, only con is it has to be injected subQ)

62
Q

IVC filter

A

Used in patients who have contraindication to anticoagulant therapy for DVT prevention, used to catch clots

63
Q

A fib causes a loss of ____ that contributes up to 25% of cardiac output

A

Atrial kick

64
Q

4 months of persistent Afib can result in…

A

….myolysis of cells, can make conversion to normal sinus rhythm much more difficult

65
Q

Source of most afib origin foci can be found in the…

A

…pulmonary veins

66
Q

Hemodynamically unstable patients with acute afib require this treatment (1)

A

direct cardioversion (synchronized)

67
Q

Hemodynamically stable patients with acute afib require this treatment (4)

A

pharmacological approach by drugs including digoxin, IV dilitiazem or verapamil, and B blockers

68
Q

CHA2DS2VASc definition

A

A calculator to determine risk of stroke in afib patients where points are awarded to determine level of risk and justify indications for anticoagulation use (a score of 1 can indicate ASA, but 2 or more requires other anticoagulants)

69
Q

Pradaxa (dabigatran) function

A

Direct thrombin (IIa) inhibitor that is used to prevent stroke in afib patients without need to check PT/INR

70
Q

Xarelto (rivoraxaban) function

A

Factor Xa inhibitor used to prevent stroke in afib patients without needing PT/INR check

71
Q

Amiodarone negative toxic side effects (5)

A
  • pulmonary toxicity
  • hyper//hypothyroidism
  • pulmonary fibrosis (most common)
  • liver toxicity
  • proarrhythmias
72
Q

Dronedarone function

A

Similar function to amiodarone but non iodinated and thus removes its bad side effects (decreases stroke, hospitalization, and death)

73
Q

4 classes of antiarrhythmic drugs

A

I (ABC) - Na+ Channel blockers
II - B blockers
III - K+ channel blockers
IV - Ca2+ channel blockers

74
Q

Shock definition

A

Physiologic state characterized by significant reduction in systemic tissue perfusion resulting in decreased oxygen delivery to the tissues, cellular hypoxia and derangement of local and eventually systemic biochemical processes

75
Q

Starling’s law

A

Amount of tension put on the ventricles by the filling of blood will correlate to the contractility generated by the ventricles

76
Q

5 categories of shock

A
  • Cardiogenic (heart muscle problem)
  • hypovolemic (due to hemorrhage or hypovolemia)
  • anaphylactic (allergic mediated third space sequestering)
  • septic (blood stream infection)
  • Neurogenic (caused by damage to NS regulation)
77
Q

2 primary drugs for cardiogenic shock

A

Intense inotropes such as

  • Dopamine
  • dobutamine
78
Q

Dopamine at small, medium, and large doses effects

A
  • Small renal vasodilation
  • Medium increased inotropy of heart
  • Large increase peripheral vascular resistance (vasoconstrict)
79
Q

Cardinal findings of shock (5)

A
  • hypotension (dropped more than 40mmHg)
  • oliguria
  • mental status changes
  • cool clammy skin
  • metabolic acidosis
80
Q

SIRS

A

Systemic inflammatory response syndrome, extreme physiological reaction to trauma, burns, or other things characterized by tachycardia, fever, rapid respiration, and abnormal WBC count that when in the presence of infection can result in sepsis

81
Q
  • Low preload requires…
  • high preload requires…
  • Increased SVR requires…
  • Decreased contractility requires…
A
  • …fluids
  • …diuretics/venodilators
  • …BP reduction (ACEI or ARB)
  • …Positive inotropic agents such as dopamine, dobutamine, epi or norepi
82
Q

Increasing preload has what effect on contraction strength?

Increasing afterload has what impact on stroke volume?

A
  • Increases contraction strength (frank starling law)
  • Decreases stroke volume-
83
Q

Types of CIEDs (cardiovascular implantable electronic device) (4)

A
  • pacemakers
  • implantable cardioverter-defibrillator (ICD)
  • implantable loop recorder
  • external cardiac monitors
84
Q

Pacemakers and what 2 things are they primarily used for

A
  • Any device that delivers low dose electrical impulse or current to provide conduction to the heart, electrical signal causes cardiac contraction when myocardial electrical activity is too low or absent
  • primarily used for heart block or hemodynamic instability
85
Q

2 types of temporary pacemaker

A
  • transcutaneous (most convenient but uncomfortable, often short term)
  • transvenous (more reliable and comfortable)
86
Q

3 parts of a pacemaker

A
  • pulse generator (battery with 7-15 year lifespan)
  • leads (sensors)
  • electrodes (transmit impulse)
87
Q

The 2 basic pacer functions

A

1) sensing a P wave
2) if none detected, then fire

88
Q

Asynchronous vs synchronous pacemaker

A
  • Asynchronous (fixed) gives a beat regardless of the speed of the heart itself
  • Synchronous (demand) only gives a shock when heart rate falls below 60bpm
89
Q

Indication for permanent pacemakers (its pretty cut and dry)

A

-symptoms with bradyarrhythmia with established correlation that have potential for progression to get worse

90
Q

Implantable cardioverter defibrillator and what are they used for

A
  • delivers high voltage shock to interrupt or terminate ventricular arrhythmias (that a patient can certainly feel)
  • Primarily used for rapid termination of Vfib or Vtach to increase chances of survival (prevent progression into asystole), considered first line treatment option
91
Q

ATP (anti-tachycardic pacing)

A

Synchronized impulse that results in painless termination of ventricular tachycardia without having to undergo shock from defibrillation (still has that option as backup if it doesn’t work)

92
Q

Cardioversion

A

Synchronized*** impulse delivered at peak of the R wave that is a painful shock to terminate Vtach

93
Q

Defibrillation

A

Unynchronized shock delivered randomly during the cardiac cycle used to restore normal cardiac functioning, initial shocks delivered at lower energies reduces capacitor charge time, subsequent shocks are delivered at higher energies

94
Q

What 3 sites are transvenous pacemakers inserted?

A
  • Right internal jugular vein
  • left subclavian vein
  • femoral vein
95
Q

Most common cause of mitral stenosis

A

Rheumatic heart disease

96
Q

Mitral stenosis key physical exam finding description

A

Opening snap after S2 and high pitched murmur heard best at the apex

97
Q

Midsystolic click is diagnostic of…

A

…mitral valve prolapse

98
Q

Why would a Transesophageal echo be preferred over a transthoracic?

A

In a patient we want to cardiovert immediately, we can confirm there is no clot very quickly to ensure cardioversion is a safe choice to not dislodge an embolism

99
Q

Unsynchronized cardioversion is done in…

A

…cardiac arrest

100
Q

don’t do unsynchronized cardioversion in heart with normal sinus rhythm or else…

A

…could put into fatal arrhythmia

101
Q

amiodarone is a ___ stage treatment for afib, vfib, or vtach

A

end, don’t do it first line ever, rather cardiovert first

102
Q

Virtually all drugs used to treat arrhythmias can ____ arrhythmias or ____ them

A

create new, worsen

103
Q

Myocardial cell (and his-purkinje system) action potential mech of action

A
  • AP propagated down stream causing Na+ voltage gated channels to open
  • Na+ influx
  • K+ efflux
  • Ca2+ influx causing plateau and prolongation
  • K+ efflux continues causing repolarization
  • Active transporters reset ion conc. to resting potential
104
Q

Pacemaker cell action potential mech of action

A
  • Spontaneous opening (after leaky channels shift gradient) of Ca2+ channels allowing influx
  • K+ efflux repolarizes
  • Active transporters reset to “resting” potential that is unstable due to leaky Na and K+ channels
105
Q

Reentry mechanism

A

In an area of one way block, the action potential goes from a separate branch and then goes retrograde thru the area of the one way block to continue re-stimulating the muscle cells in that area of the block but at a later moment in time

106
Q

Antiarrhythmics can have 2 effects on blocks and reentrant mechanisms

A
  • eliminate the block
    • convert the block to a 2 way block to prevent reentry mechanism
107
Q

Sodium channel blockers function, the 3 subclasses, and a drug in each subclass

A

Include biggest group of antiarrhythmic drugs that produce a blockade of cardiac sodium channels slowing conduction in atria, ventricles, and purkinje system including 1A quinidine, 1B lidocaine, and 1C flecanide

108
Q

B blockers antiarrhythmic function and 2 examples

A

Reduce Ca2+ entry during fast and slow potentials reducing automaticity of the pacemaker cells and reducing contractility including propranolol, acebutolol

109
Q

Drugs that delay repolarization (class III antiarrhythmics)

A

Blockade K+ channels, delay repolarization of fast channels, prolong AP duration and refractory period, examples include amiodarone, dronedarone

110
Q

Digoxin and adenosine function

A

2 drugs that do not fit into any other classes of antiarrhythmics, both drugs decrease conduction thru AV node and reduce automaticity in SA node

111
Q

Atrial flutter treatment of choice

A

-DC cardioversion almost always converts to normal sinus rhythm

112
Q

Prior to cardioversion for atrial fib, a patient needs to be given ___ 3-4 weeks before and for 1-2 weeks after

A

anticoagulants

113
Q

Sustained ventricular tachycardia treatments of choice (3)

A

-cardioversion
-IV procainamide if fails
-IV lidocaine or amiodarone are alternatives
-

114
Q

Torsades des pointes can be caused by class ___, ___, and ____ antiarrhythmics, and is treated with _____ plus _____

A

IA, III, and IV magnesium, cardioversion

115
Q

Supraventricular vs ventricular arrhythmia treatment

A

Supra are usually benign, treatment goal to terminate arrhythmia or prevent excessive atrial beats from reaching ventricles, ventricular arrhythmias need to be treated

116
Q

Quinidine drug class and function, ADR’s (3), drug interactions

A
  • Class IA
  • Drug most commonly used to treat supraventricular tach and atrial flutter/fib, blockades sodium channels, slows impulse of conduction delaying depolarization, strongly anticholinergic blocking vagal imput on heart and thus must be pre-treated with AV conduction suppressant such as verapamil, or B blocker

Adverse effects include diarrhea, cinchonism (tinnitus, headache, etc with one dose), QT prolongation, require pretreatment with anticoagulants

Intensifies effect of atropine, can double digoxin levels

117
Q

Phenytoin (dilantin) function

A

Antiseizure drug used to treat digoxin induced arrhythmia, reduces automaticity in ventricles, has little or no effect on EKG, differs in that it increases AV nodal conduction

118
Q

Flecainide drug class and function

A
  • Class IC agent
  • active against ventricular and supraventricular arrhythmias, decreases cardiac conduction and increases absolute refractory period, prolongs the PR interval and widens QRS complex, pro-arrhythmic effects such as in patients with asymptomatic vtach associated with MI, can precipitate heart failure so should not be combined with other agents that decrease contractile effect, should be used for situations without safer drug options
119
Q

Procainamide function

A

Class IA agent Similar to quinidine but CAN terminate vtach and vfib, but has serious side effects such as SLE like syndrome, blood dyscrasia, QT prolongation

120
Q

Disopyramide function

A

Class IA agent Actions similar to quinidine, but ADR’s such as anticholinergic response common and limits use

121
Q

Amiodarone drug class, function, and ADR’s (3)

A
  • Repolarization delayer class III antiarrhythmic
  • lasts for a long time and higly effective against all types of arrhythmia, approved for long term therapy for 2 life threatening ventricular arrthymias in patients who have not responded to other agents, most effective drug for Afib even tho not approved for this use to convert to sinus rhtynm and maintain it
  • ADR’s include pulmonary toxicity, sinus bradycardia, and thyroid toxicity (T4 to T3 conversion)
122
Q

Dronedarone (multaq) function

A

Derivative of amiodarone that is noniodinated but also less effective, approved for PO treatment of aflutter and paroxysmal or persistent afib but not permanent atrial fib, doubles risk of death in patients with hf or permanent afib

123
Q

Verapamil and dilitiazem drug class, function, ADR’s (4), and drug interactions (2) (anti-arrhythmic)

A
  • Class IV antiarrhythmic agent
  • Reduce SA node automaticity, delay av conduction, reduce myocardial contractility, slows ventricular rate in pats with atrial fib or flutter, terminates supraventricular tach cause by av nodal reentrant circuit
  • ADR’s include hypotension and vasodilation, bradycardia, AV block
  • Drug interactions with digoxin amplify it, B blockers are contraindicated because they produce exaggerated effect when combined
124
Q

Adenosine (adenocard) DOC for what condition

A

IV drug of choice for terminating paroxysmal supraventricular tach

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