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
Propafenone Adverse Effects
Dizziness, disturbance in taste
26
Beta 1 vs Beta 2 receptors
27
Beta Blockers Adverse Effects
Hypotension Bradycardia AV block Suppress hypoglycemia symptoms
28
First Generation Beta Blockers
Propranolol Nonselective: Beta 1 and Beta 2
29
Second Generation Beta Blockers
Atenolol, Metoprolol Relatively selective for Beta 1
30
Third Generation Beta Blockers
Labetolol, Carvedilol Selective for Beta 1 Also cause vasodilation
31
Potassium Channel Blockers Examples
Amiodarone, Ibutelide, Dofetilide, Sotalol
32
Ibutelide Indications and Adverse Effect
Indications: atrial fibrillation and flutter Adverse Effect: Prolonged QT--\> Torsades de Pointes Do NOT give to patients with pre-existing prolonged QT
33
Dofetilide Indications and Adverse Effects
Indicated only in Afib or Aflutter to NSR, can be used with depressed EF Adverse effects: prolonged QT--\> torsades de pointes
34
Sotalol Mechanism of Action and Indications
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
35
Sotalol Adverse Effects
Remember it has both class II and class III Class II: fatigue, bradycardia Class III: Torsades de Pointes
36
Amiodarone Class and Mechanism of Action
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
Amiodarone Indications
▪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
Amiodarone Adverse Effects
▪Bradycardia, AV block, HF ▪Pulmonary fibrosis ▪Hepatic failure ▪Thyroid dysfunction ▪Corneal microdeposits ▪Photosensitivity ▪Blue-gray skin ▪Neutropenia
39
Verapamil and Diltiazem Mechanism of Action
Calcium Channel Blockers: Class IV antiarrhythmic agents Slow AP upstroke in AV nodal cells, leading to slowed conduction velocity through AV node
40
Verapamil and Diltiazem Indications and Adverse Effects
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
Adenosine Adverse Effects
Very short half life (less than 10 seconds) Bronchoconstriction, CP, flushing, excessive SA or AV nodal inhibition
42
Magnesium Indications
Replacement therapy, Digoxin toxicity Drug of Choice for Torsades de Pointes
43
Vassopressor Definition
Agent that causes vascular constriction
44
Inotrope Definition
Agent that affects force of heart’s contraction
45
Chronotrope Definition
Agent that increases heart rate by affecting the electrical system and neuronal stimulation to the heart
46
Domotrope Definition
Agent that increases the conduction speed in the heart and AV node
47
Lusitrope Definition
Agent that increases diastolic relaxation
48
Bathmotropy Definition
Refers to myocardial excitability
49
Which receptors are vasoactive?
▪Catecholamine receptors ▪Dopamine receptors ▪Vasopressin receptors ▪Angiotensin II receptors
50
Catecholamine Receptors Alpha 1 vs Alpha 2
51
Catecholamine Receptors Beta 1 vs Beta 2 vs Beta 3
52
Dopamine Recpeptors
Promotes vasodilation Promotes diuresis (because of vasodilation of renal arteries)
53
Vassopressin Recpetors
54
Angiotensin II (type I) receptors
Promotes vasoconstriction Promotes aldosterone production Promotes vasopressin release Decreases renal blood flow
55
Phenylephrine Mechanism of Action
Works by stimulating alpha-1 adrenergic receptors in peripheral vasculature
56
Norepinephrine Mechanism of Action
Potent alpha-adrenergic agonist, with mild beta agonism Acts as a potent vasoconstrictor, risk for tissue necrosis
57
Epinephrine Receptor Responses
Agonist for all types of adrenergic receptors ▪Lower concentrations—beta effects predominate ▪Increasing doses—alpha 1 agonism present
58
Dobutamine Mechanism of Action
Preferentially activates beta 1 receptors with 3 times more affinity than beta 2 receptors Also has mild alpha agonist activity
59
Isoprotorenol Mechanism of Action
▪Synthetic non-selective beta-agonist ▪Increases inotropy ▪More chronotropic effect than Dobutamine ▪Less selective beta 2 agonism ▪No alpha activity
60
Dopamine Mechanism of Action
Acts directly on dopamine receptors in renal, mesenteric and coronary vascular beds causing vasoconstriction Hemodynamic effects due to conversion into NE and Epi
61
Effects of Vasopressin
Increased free water resorption from collecting tubules in kidney Vasoconstriction of peripheral vasculature
62
Which antihypertensives should you give with HF?
ACEI, BB, ARB, AA, Thiazide
63
Which antihypertensives should you give post MI?
ACEI, BB, AA
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Which antihypertensives should you give with high CVD risk?
Thiazide, ACEI, BB, CCB
65
Which antihypertensives should you give with diabetes?
Thiazide, ACEI, ARB, CCB
66
Which antihypertensives should you give with CKD?
ACEI, ARB
67
Which antihypertensives should you give for recurrent stroke prevention?
Thiazide, ACEI
68
Relative contraindications for antihypertensive therapy
▪Hyperkalemia: Aldosterone Antagonists not good ▪Bradycardia: BB not recommended ▪Uncontrolled Asthma: BB not recommended ▪ESRD: HCTZ does not work
69
Pharm agent for atrial fibrillation rate control
BB, CCB, Digoxin Also need antithrombotic therapy (warfain or aspirin 325)
70
Pharm agent for atrial fibrillation rhythm control
▪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
Pharm agent for atrial flutter rate control
BB, CCB, Digoxin
72
Pharm agent for atrial flutter rhythm control
Catheter ablation of the “Isthmus” in the right atrium
73
Pharm agents AVNRT
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
Pharm agents AVRT
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
Pharm agents Monomorphic VT
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
Torsades de Pointes
▪Magnesium ▪Isoproterenol ▪Overdrive pacing ▪Shock
77
Angina Therapies
▪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
What is MONA?
Morphine, oxygen, nitrate, aspirin Given for acute STEMI
79
Acute STEMI management
* MONA * Beta Blocker * Reperfusion: PCI or thrombolytic * Antithrombotics
80
Chronic STEMI/NSTEMI Management
▪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
Acute Decompensated HF management
* Diuresis * Vasodilators * Uptitrate HF meds * Inotropes
82
Chronic HFrEF management
▪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
Chronic HFpEF management
▪Volume Control ▪BP control
84
Lipid lowering therapies
Statins are first line Secondline (contraversial): colesevelam, niacin, ezetimibe
85
Elevated triglyceride management
Check for DM and hypothyroidism If trigylcerides over 500: start fibrates and omega 3 fatty acids d/t risk for pancreatitis
86
Cardiac output =
Heart rate x Stroke volume