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2022 Adv Pharm Faculty Landing Page > Acute Cardiac > Flashcards

Acute Cardiac Flashcards

1
Q

Digoxin Mechanism of Action

A

Sodium-Potassium ATPase blocker leading to inhibition of SNS and decreases automacity of AV node

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2
Q

Digoxin indications

A

Atrial fibrillation and heart failure

Control ventricular rate in patients with prolonged atrial fibrillation

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3
Q

Digoxin Adverse Drug Effects

A

Arrhythmias

Nausea and vomiting

Yellow/green visual auras

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4
Q

Types of Vasodilators and Examples

A
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5
Q

Hydralazine Indications and Mechanism of Action

A

Acute antihypertensive (IV)

4th line agent for chronic HTN

Used in conjunction with nitrates as chronic therapy in HFrEF

Mechanism of action is unknown, somehow cause smooth muscle relaxation resulting in arteriolar vasodilation

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6
Q

Minoxidil Indications and Mechanism of Action

A

4th line agent for chronic HTN

Increases Potassium channel activity in smooth muscle leading to membrane hyperpolarization and relaxation and arteriolar vasodilation

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7
Q

Minoxidil Adverse Effects

A

Hair growth

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8
Q

Calcium Channel Blockers Indications

A

Angina

Coronary artery spasm

HTN

Supraventricular arrhythmia (action at AV node—Verapamil, Diltiazem)

**No benefit in heart failure**

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9
Q

Nitrates Mechanism of Action

A

Mostly venodilation, some arteriolar dilation in coronary beds

Causes arteriolar dilation in face (flushing)

Decreases preload and at higher doses afterload

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10
Q

Sodium Nitroprusside Indications

A

Drug of choice for HTN emergency

Acute decompensated HF

Decreases both preload and afterload

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11
Q

Central α2 agonists Adverse Effects

A

Sedation

Rebound HTN with abrupt discontinuation

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12
Q

Diuretic drug classes and examples

A
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13
Q

Classes of antiarrythmic agents

A

▪Class I—Na + channel blockers

▪Class II—Beta-adrenergic receptor blockers

▪Class III—K + channel blockers

▪Class IV-Ca 2+ channel blockers

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14
Q

Quinidine Mechanism of Action

A

Blocks transmitter release from the vagus nerve

Can increase conduction velocity through the AV node

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15
Q

Quinidine Adverse Effects

A

Nausea, light headedness, headache, tinitis

Drug interaction with dixogen can lead to toxicity, need to monitor K+

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16
Q

Procainamide Indications

A

Supraventricular and ventricular arrhythmias

Conversion of new onset Afib to NSR,

Decrease likelihood of re-entry arrhythmias in acute MI

Can be used for VT—but not preferred drug

**Avoid with hyperkalemia (toxicity)

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17
Q

Procainamide Adverse Effects

A

Reversible SLE with chronic use

Prolonged QT

Torsades de pointes

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18
Q

Lidocaine Mechanism of Action and Indications

A

Alters the ventricular action potential by blocking Na+ channels which causes Na+ channels to remain open or inactive longer.

Can shorten repolarization, but DOES NOT prolong QT interval

Indicaitons: emergency ventricular arrhythmias, VT and PVC in stable patients

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19
Q

Lidocaine Adverse Effects

A

▪Slurred speech, tinnitus, hearing impairment, seizures, muscle twitching

▪Altered mental status, confusion

▪Blurred vision

▪Heart blocks

▪Altered AV conduction

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20
Q

Mexiletine Mechanism of Action and Indications

A

Blocks Na+ channels thereby altering ventricular action potential

DOES NOT prolong QT interval and it lacks vagolytic side effects

Indications: emergency ventricular arrhythmias

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21
Q

Mexiletine Adverse Effects

A

Nausea and tremor

Take with food to reduce side effects

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22
Q

Flecainide Indications and Contraindications

A

Indications: SVT, Atrial fibrillationn, PVC

Contraindications: structural heart disease and post MI

Should only be given to patients with normal EF

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23
Q

Flecainide Adverse Effects

A

Dizziness, headache, visual distrubance

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24
Q

Propafenone Mechanism of Action and Indications

A

Sodium channel blocker (most potent) with weak beta blocking activity

Indications: SVT, Atrial fibrillation, PVC

Should only be given to patients with normal EF

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25
Q

Propafenone Adverse Effects

A

Dizziness, disturbance in taste

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26
Q

Beta 1 vs Beta 2 receptors

A
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27
Q

Beta Blockers Adverse Effects

A

Hypotension

Bradycardia

AV block

Suppress hypoglycemia symptoms

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28
Q

First Generation Beta Blockers

A

Propranolol

Nonselective: Beta 1 and Beta 2

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29
Q

Second Generation Beta Blockers

A

Atenolol, Metoprolol

Relatively selective for Beta 1

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30
Q

Third Generation Beta Blockers

A

Labetolol, Carvedilol

Selective for Beta 1

Also cause vasodilation

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31
Q

Potassium Channel Blockers Examples

A

Amiodarone, Ibutelide, Dofetilide, Sotalol

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32
Q

Ibutelide Indications and Adverse Effect

A

Indications: atrial fibrillation and flutter

Adverse Effect: Prolonged QT–> Torsades de Pointes

Do NOT give to patients with pre-existing prolonged QT

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33
Q

Dofetilide Indications and Adverse Effects

A

Indicated only in Afib or Aflutter to NSR, can be used with depressed EF

Adverse effects: prolonged QT–> torsades de pointes

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34
Q

Sotalol Mechanism of Action and Indications

A

Mixed class II and III

▪Non-selectively antagonizes β-receptors (Class II action)

▪Blocks K+ channels (Class III action)

Indications: atrial fibrillation/flutter, severe ventricular arrhythmias

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35
Q

Sotalol Adverse Effects

A

Remember it has both class II and class III

Class II: fatigue, bradycardia

Class III: Torsades de Pointes

36
Q

Amiodarone Class and Mechanism of Action

A

Mainly Class III but also acts as Class I, II, IV arrhythmic

Alteration of lipid membrane in which ion channels and receptors are located

37
Q

Amiodarone Indications

A

▪Preferred drug for hemodynamically unstable ventricular tachycardia or fibrillation

▪Highly effective in prevention of recurrent parxosymal atrial fibrillation or flutter

▪Preferred drug in ACLS VT/VF algorithm

38
Q

Amiodarone Adverse Effects

A

▪Bradycardia, AV block, HF

▪Pulmonary fibrosis

▪Hepatic failure

▪Thyroid dysfunction

▪Corneal microdeposits

▪Photosensitivity

▪Blue-gray skin

▪Neutropenia

39
Q

Verapamil and Diltiazem Mechanism of Action

A

Calcium Channel Blockers: Class IV antiarrhythmic agents

Slow AP upstroke in AV nodal cells, leading to slowed conduction velocity through AV node

40
Q

Verapamil and Diltiazem Indications and Adverse Effects

A

Used for treating paroxysmal SVT

Increases plasma digoxin level by competing with Digoxin for renal excretion

Administration of IV Verapamil in patients taking β-blockers can precipitate severe heart failure

41
Q

Adenosine Adverse Effects

A

Very short half life (less than 10 seconds)

Bronchoconstriction, CP, flushing, excessive SA or AV nodal inhibition

42
Q

Magnesium Indications

A

Replacement therapy, Digoxin toxicity

Drug of Choice for Torsades de Pointes

43
Q

Vassopressor Definition

A

Agent that causes vascular constriction

44
Q

Inotrope Definition

A

Agent that affects force of heart’s contraction

45
Q

Chronotrope Definition

A

Agent that increases heart rate by affecting the electrical system and neuronal stimulation to the heart

46
Q

Domotrope Definition

A

Agent that increases the conduction speed in the heart and AV node

47
Q

Lusitrope Definition

A

Agent that increases diastolic relaxation

48
Q

Bathmotropy Definition

A

Refers to myocardial excitability

49
Q

Which receptors are vasoactive?

A

▪Catecholamine receptors

▪Dopamine receptors

▪Vasopressin receptors

▪Angiotensin II receptors

50
Q

Catecholamine Receptors

Alpha 1 vs Alpha 2

A
51
Q

Catecholamine Receptors

Beta 1 vs Beta 2 vs Beta 3

A
52
Q

Dopamine Recpeptors

A

Promotes vasodilation

Promotes diuresis (because of vasodilation of renal arteries)

53
Q

Vassopressin Recpetors

A
54
Q

Angiotensin II (type I) receptors

A

Promotes vasoconstriction

Promotes aldosterone production

Promotes vasopressin release

Decreases renal blood flow

55
Q

Phenylephrine Mechanism of Action

A

Works by stimulating alpha-1 adrenergic receptors in peripheral vasculature

56
Q

Norepinephrine Mechanism of Action

A

Potent alpha-adrenergic agonist, with mild beta agonism

Acts as a potent vasoconstrictor, risk for tissue necrosis

57
Q

Epinephrine Receptor Responses

A

Agonist for all types of adrenergic receptors

▪Lower concentrations—beta effects predominate

▪Increasing doses—alpha 1 agonism present

58
Q

Dobutamine Mechanism of Action

A

Preferentially activates beta 1 receptors with 3 times more affinity than beta 2 receptors

Also has mild alpha agonist activity

59
Q

Isoprotorenol Mechanism of Action

A

▪Synthetic non-selective beta-agonist

▪Increases inotropy

▪More chronotropic effect than Dobutamine

▪Less selective beta 2 agonism

▪No alpha activity

60
Q

Dopamine Mechanism of Action

A

Acts directly on dopamine receptors in renal, mesenteric and coronary vascular beds causing vasoconstriction

Hemodynamic effects due to conversion into NE and Epi

61
Q

Effects of Vasopressin

A

Increased free water resorption from collecting tubules in kidney

Vasoconstriction of peripheral vasculature

62
Q

Which antihypertensives should you give with HF?

A

ACEI, BB, ARB, AA, Thiazide

63
Q

Which antihypertensives should you give post MI?

A

ACEI, BB, AA

64
Q

Which antihypertensives should you give with high CVD risk?

A

Thiazide, ACEI, BB, CCB

65
Q

Which antihypertensives should you give with diabetes?

A

Thiazide, ACEI, ARB, CCB

66
Q

Which antihypertensives should you give with CKD?

A

ACEI, ARB

67
Q

Which antihypertensives should you give for recurrent stroke prevention?

A

Thiazide, ACEI

68
Q

Relative contraindications for antihypertensive therapy

A

▪Hyperkalemia: Aldosterone Antagonists not good

▪Bradycardia: BB not recommended

▪Uncontrolled Asthma: BB not recommended

▪ESRD: HCTZ does not work

69
Q

Pharm agent for atrial fibrillation rate control

A

BB, CCB, Digoxin

Also need antithrombotic therapy (warfain or aspirin 325)

70
Q

Pharm agent for atrial fibrillation rhythm control

A

▪Flecainide, Propafenone (Class IC): Structurally normal hearts, younger patients

▪Amiodarone, Dofetilide, Sotalol (Class III): Structurally abnormal hearts or nomal hearts. Dose adjust Dofetilideand Sotalol for GFR. Monitor QTc.

▪Amiodarone: Usually used for older patients (risk of lung, liver, thyroid toxicities)

▪Ibutilide (Class III): IV; used for acute cardioversion

71
Q

Pharm agent for atrial flutter rate control

A

BB, CCB, Digoxin

72
Q

Pharm agent for atrial flutter rhythm control

A

Catheter ablation of the “Isthmus” in the right atrium

73
Q

Pharm agents AVNRT

A

Acute: Adenosine, BB, CCB

Chronic: AV nodal blocking agent—BB, CCB, Digoxin can all be used

BB are by far the most commonly used

Ablation of slow pathway also option

74
Q

Pharm agents AVRT

A

Acute: Narrow complex—>Adenosine. If wide complex, be careful that it is not VT

▪Slowing down AV node conduction—very dangerous

▪AV nodal blockers can be used in conjunction with Flecainide or Propafenone for rhythm control in AVRT

75
Q

Pharm agents Monomorphic VT

A

Amiodarone (III)—Acute or Chronic setting

Sotalol also useful (Class III)

Lidocaine (IB) IV in acute MI (second line to Amiodarone)

Beta-blockers

Chronic Rx: Usually adjuncts to defibrillators—reduce shocks

Flecainide and Propafenone are Contraindicated (Class IC)

Class IA drugs are rarely used

76
Q

Torsades de Pointes

A

▪Magnesium

▪Isoproterenol

▪Overdrive pacing

▪Shock

77
Q

Angina Therapies

A

▪Anti-ischemic agents: Beta blockers, CCB, Nitrates

▪Anti-platelet agents: Aspirin, Clopidogrel or Thienopyridine if ASA intolerant

▪Lipid lowering therapy: Statin for LDLc < 100 or <70 mg/dL

▪Consider ACE-I or ARB for beneficial effect of CAD progression

78
Q

What is MONA?

A

Morphine, oxygen, nitrate, aspirin

Given for acute STEMI

79
Q

Acute STEMI management

A
  • MONA
  • Beta Blocker
  • Reperfusion: PCI or thrombolytic
  • Antithrombotics
80
Q

Chronic STEMI/NSTEMI Management

A

▪Aspirin

▪Clopidogrel or other thienopyridine

▪For dual antiplatelet for any stent

▪For indication of NSTEMI or STEMI itself

▪Statin regardless of lipid level

▪BB

▪ACEI or ARB

81
Q

Acute Decompensated HF management

A
  • Diuresis
  • Vasodilators
  • Uptitrate HF meds
  • Inotropes
82
Q

Chronic HFrEF management

A

▪Beta-blockers

▪ACEI or ARB

▪Diuretic (usually loop)

▪Aldosterone antagonist—Class II or III Sx, ~ EF < 35%

▪Hydralazine + Nitrate—use also in patients who can’t tolerate ACEI or ARBs

▪Digoxin— helps reduce hospitalization

83
Q

Chronic HFpEF management

A

▪Volume Control

▪BP control

84
Q

Lipid lowering therapies

A

Statins are first line

Secondline (contraversial): colesevelam, niacin, ezetimibe

85
Q

Elevated triglyceride management

A

Check for DM and hypothyroidism

If trigylcerides over 500: start fibrates and omega 3 fatty acids d/t risk for pancreatitis

86
Q

Cardiac output =

A

Heart rate x Stroke volume

2022 Adv Pharm Faculty Landing Page (22 decks)

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