Cardiac drugs Flashcards by Shay Edgeston

What is the MOA of Beta Blockers?

Blocks catecholamine binging to Beta in cardiac muscle

Decreases contractility, HR & conduction velocity

Increases relaxation

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Smooth muscle contraction is related to

Beta-2

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Abrupt withdrawal of beta blockers can cause

Rebound HTN
Tachycardia
Increased Contractility

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First Generation Beta Blockers are

Non-selective for Beta 1 & 2

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Examples of Non-Selective Beta Blockers

Carvedilol
Labetalol
Propranolol
Sotalol
Timolol

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Which Beta blocker are Beta 1 selective?

Atenolol
Esmolol
Metoprolol

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How do you treat over-dose of a Beta Blocker?

Atropine
B1 agonist
Glucagon
Ca+ Chloride
Pacemaker
Vasopressors

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Beta Blocker & the newborn

Crosses the Placenta, causing bradycardia, HOTN & decrease in blood sugar in Newborns

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Side effects of Beta Blockers

Increased airway resistance
Bronchoconstriction
Risk depressed ventilation
Fatigue
Memory loss

Decreased Renin=Na+ & water loss

Decreased glycogenolysis=Hypoglycemic

Blocked NaKATPase=Hyperkalemia

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Which population should you caution using Beta Blockers

Asthma & COPD

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Esmolol is a pure

Beta 1 antagonist

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How is Esmolol metabolized?

RBC Esterase (hydrolysis)

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Dose of Esmolol?

0.2-0.5mg/kg IV

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What is the dose of Metoprolol?

1-5mg

1-15 MAX mg IV

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What is the duration of Metoprolol?

4-8 hrs

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Labetalol selectivity

Non-selective Beta

Selective for Alpha 1 blockade

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What is the dose of Labetalol?

0.1-0.25mg/kg

2mg/min infusion

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What is the dose of Propranolol?

0.25mg
2-5mg MAX

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Propranolol will decrease the clearance of

Amide Local & pulmonary uptake of Fentanyl

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What is the dose of Atenolol?

25-200mg PO

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Side effects of Atenolol

Ortho HOTN
SOB
Edema`

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What is the dose of Carvedilol?

6.25-100mg PO

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What are the side effects of Carvedilol

Hyperglycemia
Ortho HOTN
Bronchospasm
Edema
Fatigue

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What are the MOA of Alpha Blockers

Binds on vascular smooth muscle
Antagonism at Alpha-2 receptors
Increases release of NE

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What are the uses of Atenolol?

HTN emergencies Extravasation BPH Raynaud's

What is the dose of Phentolamine, an Alpha Blocker

5-10mg IV (has competitive antagonism)

Phenoxybenzamine, an alpha blocker is

Non-competitive antagonist

Newer alpha blockers are

Alpha 1 selective Decreases BP w/o an increase in NE release

What is the MOA of Alpha-2 agonists?

(inhibitory) Binds & activates presynaptic Alpha 2 adrenergic receptors Decreases presynaptic Ca+ levels Inhibits NE release

Alpha-2 agonists will decrease

Cardiac Output HR Contractility Vascular tone/SVR Arterial Pressure

What are the side effects of Alpha 2 agonists?

Sedation Brady Fluid retention & edema

How is Alpha 2 agonists reversed?

Labetalol Nitroprusside Hydralazine

Clonidine, an Alpha 2 agonists can decrease MAC by

15-50%

What is the black box warning of Clonidine

Hemodynamic instability

What is the MOA of CCB?

Prevents release of internal Ca+ stores Binding keeps Ca+ channel in inactivated/closed state

CCB primary effect

Arterial resistance

CCB effects on smooth muscle

Smooth muscle relaxation (decrease in SVR)

Which CCB are non dihydropyridines?

Verapamil Diltiazem (cardiac sledctive)

What is the dose of Nicardipine, a dihydropyridine CCB?

3-5mg/hr 15mg/hr MAX

Which CCB are dihydropyridines?

Amlodipine Nicardipine Nifedipine Nimodipine (selective for vascular smooth muscle)

When will vasodilation occur after Nicardipine administration

10-15min

What is needed with a Nicardipine infusion?

Central line/large PIV Change site Q12h

How is Clevidipine, a dihydropyridine CBB metabolized?

Plasma esterase, which causes a delay in metabolism with a patient with Pseudocholinesterase deficiency

What is the dose of Clevidipine, a dihydropyridine CBB

1-2mg/hr, & then you can double Q90sec Average dose is 4-8mg/hr

What are side effects of Clevidipine, a dihydropyridine CBB

Flushing HA Reflex tachy Potentiates NMB

What is a common side effect of dihydropyridine

Reflex tachycardia Additive effects w/IA & BB Potentiates NMB

What are common side effects of non-dihydropyridines

Excessive Bradycardia & AV node blockade Depressed contractility

What is the treatment choice of BB & CCB overdose

Brady: Atropine & Isoproterenol AV block: Atropine, Isoproterenol & pacing HF: Inotropes & Diuretics HOTN: Vasopressors (dopamine & norepi) Glucagon, pacing, CPR

PDE-3 inhibitors increases

cAMP

PDE-3 inhibitors will increase

Contractility Stroke Volume EF Cardiac output

PDE-3 inhibitors will decrease

Preload & PCWP

What are examples of PDE-3 inhibitors

Milrinone Inamrinone

PDE-5 inhibitors increase

cGMP, causing vasodilation

What is the MOA of PDE-5 inhibitors

NO causes an increase in the formation of cGMP, which activates K+ channels & INHIBITS Ca+ entry

What are examples of PDE-5 inhibitors

Sildenafil Tadalafil Vardenafil

What is the dose of Milrinone, a PDE-3 inhibitor

Loading 50mcg/kg (10min) 0.375-0.75mcg/kg/min

What are the side effects of PDE-3 inhibitors?

HA V. arrhythmias HOTN

What are side effects of PDE-5 inhibitors

HA Flushing Exaggerated HOTN Impaired coronary perfusion with Nitrodilators

What is the MOA of ACE inhibitors?

Blocks the conversion of angiotensin to angiotensin 2 by ACE Blocks ACE's breakdown of bradykinin

ACE inhibitors end in

-pril

ACE inhibitors inhibits the secretion of

Aldosterone

ACE inhibitors will decrease

Ventricular afterload & overload

What are the side effects of ACE ihibitors

Dry cough Hyperkalemia due to aldosterone respiratory congestion Rhinorrhea HOTN Angioedema

What is the dose for Enalapril?

1.25mg IV over 5 min (Q6H MAX 5 mg & Q6h

What is the MOA of ARBs

Blocks Angiotensin 2 binding to AT-1 receptors

ARBs end in

-ratan

What is Vasoplegic Syndrome?

Common in cardiac surgery, which is severe HOTN refractory to catecholamine therapy

What is the MOA of Nitrodilators?

Increase in Nitric Oxide in CV system Increase enzymatic breakdown to NO (nitrates)

What are the cardiac effects of Nitrodilators?

Reduced preload & afterload & O2 demand

Increased cGMP in smooth muscle will cause

Relaxation

Dose of Sodium Nitroprusside

0.5-10mcg/kg/min IV NEVER INFUSE MAX DOSE >10min

Metabolism of sodium nitroprusside can cause

Cyanide & Cyanmethemoglobin Cyanide toxicity--> lactic acidosis & hyperoxemia

Effects/Side effects of sodium nitroprusside

Increased CBF & ICP Decreased hypoxic pulmonary vasoconstriction Inhibition of PLT aggregation

How do you treat cyanide toxicity

Sodium nitrite, thiosulfate Dialysis Hydrocobalamin Exchange transfusion

What is the dose of Nitroglycerin?

5-20+ mcg/min IV MAX 200mcg/min

What are the side effects of Nitroglycerine?

HA Flushing Postural HOTN Reflex tachy Toxicity Tolerance & decreased efficacy

How do you treat Methemoglobinemia

Methylene blue 1-2mg/kg

What is the MOA of Hydralazine

Direct Vasodilator Arteries/Arterioles Binds/activates K+ channels (hyperpolarization Increased renin activity in plasma

What is the dose of Hydralazine?

2-20+mg IV/IM Onset 2-20min

Side effects of Hydralazine

Angina, MI decreased pressor response to EPI Tachy Paresthesia L-T use=systemic lupus syndrome

Increase in cAMP in cardiac muscle will lead to

Contraction

A decrease in cAMP in smooth muscle will lead to

Contraction