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CVT > Module 2 - ANS/CV Pharmacology > Flashcards

Module 2 - ANS/CV Pharmacology Flashcards

1
Q

Chassaignac Tubercle

The most prominent tubercle in the neck.

The anterior tubercle of the transverse process of the ______cervical vertebra, against which the carotid artery may be compressed by the finger (i.e., carotid massage).

Extremely sensitive to stimulation during laryngoscopy.

A

6th

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2
Q

Anesthesia & the ANS

  • The ANS includes that part of the central and peripheral nervous system concerned with _________ regulation of cardiac muscle, smooth muscle, and glandular and visceral functions.
  • ANS activity refers to visceral reflexes that function below the ____ level. The ANS is also responsive to changes in somatic motor and sensory activities of the body.
  • The main effect of vagal cardiac stimulation to the heart is __________. Vagal stimulation decreases the rate of sinoatrial node discharge and decreases excitability of the AV junctional fibers, slowing impulse conduction to the ventricles.
  • A strong vagal discharge can completely arrest sinoatrial node firing and block impulse conduction to the ventricles.
A
  • involuntary
  • conscoius
  • chronotropic.
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3
Q

Anesthesia & the ANS

  • Afferent fibers from visceral structures are the first link in the ___________ of the ANS, and may relay visceral pain or changes in _________.
  • Most ANS efferent fibers are accompanied by_________ fibers that are now commonly recognized as components of the ANS.
A
  • reflex arcs; vessel stretch
  • sensory
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4
Q

Anesthesia & the ANS

  • However, the afferent components of the ANS cannot be as distinctively _________ as can the efferent nerves.
  • ANS visceral sensory nerves are anatomically ___________ from somatic sensory nerves.
  • The clinical importance of visceral afferent fibers is closely implicated in the management of ____________.
A
  • divided
  • indistinguishable
  • chronic pain states
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5
Q

Functional Anatomy

The ANS is organized into two divisions based on anatomy, physiology, and pharmacology.

Langley divided this nervous system into two parts in 1921. He retained the term sympathetic (sympathetic nervous system [SNS]) introduced by Willis in 1665 for the first part, and introduced the term “parasympathetic” (parasympathetic nervous system [PNS]) for the second.

The term ________ was adopted as a comprehensive name for both.

A

ANS

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6
Q

Functional Anatomy

  • The physiologic evidence of visceral reflexes as a result of somatic events is abundantly clear. The ANS is therefore not as __________ an entity as the term suggests.
  • Neither somatic nor ANS activity occurs in ________. The ANS organizes visceral support for somatic behavior and adjusts body states in anticipation of emotional behavior or responses to the stress of disease.
  • In brief, it organizes fight or flight responses.
A
  • distinct
  • isolation
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7
Q

Homeostatic Balance Between **Adrenergic vs. Cholinergic Effect

Table 14-1

A
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8
Q

ANS Transmission

  • Transmission of excitation across the terminal junctional sites (synaptic clefts) of the peripheral ANS occurs through the mediation of ___________.
  • Transmitters interact with receptors on the end organ to evoke a biologic response.
A

released chemicals

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9
Q

Receptors

  • An agonist is a substance that interacts with a receptor to evoke a biologic response.
  • ____,____,____,____and _____ are the major agonists of the ANS.
  • An antagonist is a substance that interferes with the evocation of a response at a receptor site by an agonist.
  • Receptors are therefore target sites that lead to a response by the effector cell when activated by an agonist.
  • Receptors are ___________ and are located in the plasma membrane.
  • Several thousand receptors have been demonstrated in a single cell. The enormity of this network becomes apparent when one considers that ∼__________ single cells can be innervated by a single neuron.
A
  • ACh, NE, EPI, DA, and ATP
  • protein macromolecules
  • 25,000
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10
Q

CV Anatomy and Physiology

  1. Calcium plays a critical role in the regulation of peripheral vessel diameter.
  2. Increased Ca+2 causes ______ and reduced intracellular Ca+2 leads to __________.
  3. G-protein cAMP and Nictric oxide cGMP —> _________.
  4. Phospholipase C —-> ________.
  5. Increased ____ and _____ increase intracellular calcium

PKA affects excitation-contraction coupling by: (4)

A

2 - vasoconstriction; vasodilation
3- vasodilate
4- Vasoconstriction
5- cAMP and protein kinase A (PKA)

  1. Inhibition of voltage-gated Ca+2 channels in the sarcolemma
  2. Inhibition of Ca+2 release from the SR
  3. Reduced sensitivity of the myofilaments to Ca+2
  4. Facilitation of Ca+2 reuptake into the sarcoplasmic reticulum via the SERCA2 pump
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11
Q

Selection of the Anesthetic

No one ideal anesthetic for patients with CAD.

Choice should depend on the extent of pre-existing myocardial dysfunction and the properties of the drugs.

Most patients with mid or even moderate dysfunction may benefit from some degree of ____________.

A

myocardial depression

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12
Q

Preload

  • Determines how well the pump is primed.
  • Directly related to _____ developed in the ventricle.
  • Filling pressure of the ventricles at the end of ________.
  • Right ventricular end-diastolic volume is the product of systemic venous return.
  • Left ventricular end-diastolic volume is the product of pulmonary circulation entering the left side of the heart.
A
  • tension
  • diastole
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13
Q

Preload

  • Frank Starling Principle: Increased myocardial fiber ______(preload) improves _________ up to a point of ultimate decompensation.
  • Preload can be measured by _______ and ______ or indirectly by _________.
A
  • length; contractility

*CVP (RVEDP),
LAP,
PCWP (LVEDP)

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14
Q

Afterload

Impedance to left ventricular outflow
Can be altered with drugs that dilate or constrict vascular beds - mostly via arterial vessels.

Arterial vasodilators _______ resistance to ventricular contraction but can also decrease _________.

A

decrease; preload

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15
Q

Afterload

Clinical indicator for right ventricular afterload is pulmonary vascular resistance (PVR)

Formula/ Range

A
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16
Q

Afterload

Left ventricular afterload is measured as systemic vascular resistance (SVR).

Formula/ Range

A
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17
Q

Contractility

Force of ventricular contraction and is defined as the ______ state of the heart.

Inotropic agents affect the contraction of the heart muscle.

Factors that influence contractility: (4)

A
  • inotropic

  • Appropriate amounts of potassium, sodium and calcium
  • Sympathetic nervous system via beta 1 receptors stimulation (increased contractility, HR, ventricular automaticity, and myocardial oxygen consumption
  • Increased levels of cyclic adenosine monophosphate (cAMP)
  • Preload and afterload
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18
Q

Cardiac output

Volume of blood that the heart ejects each minute.
CO = SV x HR

Normal =___-____

Cardiac index (CI) adjusts the CO value for an individual ________.

CI = CO divided by ________ (___-___ L/min)

3 primary factors that determine CO (SV):

A
  • 4 - 8 L/min
  • body size
  • BSA; 2.5-4.0

Preload
Afterload
Contractility

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19
Q

Myocardial Oxygen Supply & Demand

  • Myocardial oxygen supply is determined by oxygen content of _____ and _______.
  • Coronary perfusion is influenced by ________. (Slower heart rate increases diastolic time thus allowing for increased coronary perfusion)
  • _______ pressure determines coronary perfusion pressure.
  • Coronary blood flow is regulated by coronary vascular tone.
A
  • arterial blood and coronary perfusion.
  • heart rate
  • Diastolic
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20
Q

Myocardial Oxygen Supply & Demand

  • Myocardial oxygen demand is influenced by : (4)
  • Myocardial oxygen demand is increased by an increase in preload (increase in _________) and an increase in inotrophy.
  • Myocardial oxygen demand is decreased by a decrease in afterload and HR.
A
  • preload, afterload, inotrophy and heart rate
  • ventricular diameter
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21
Q

Adrenergic Receptors

  • _____________ is the neurotransmitter responsible for most adrenergic activity of the sympathetic nervous system.
  • Norepinephrine is released by ___________ sympathetic fibers at end organ tissues.
  • Action of norepinephrine is terminated by _________ into the postganglionic nerve ending.
  • Divided into alpha and beta receptors.
A
  • Norepinephrine
  • postganglionic
  • reuptake
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22
Q

Alpha 1 Receptors

  • Located in _______ muscle throughout the body.
  • Most important cardiovascular effect of alpha 1 stimulation is _________.
  • Increase in _____________.
  • Increase in ____________.
A
  • smooth
  • vasoconstriction
  • peripheral vascular resistance
  • arterial blood pressure
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23
Q

Alpha 2 Receptors

  • Located chiefly on the ______ nerve terminals.
  • Stimulation of Alpha 2 receptors creates a ______________ that inhibits further norepinephrine (NE) release. Decreases ___________.
  • Antagonism (blockage) of Alpha 2 receptors causes a enhanced release of _________ from nerve endings.

  • Note the added complexity and detail in Barash re: postsynaptic Alpha 2
A
  • presynaptic
  • negative feedback loop; vasoconstriction
  • NE
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24
Q

Beta 1 Receptors

  • Most important Beta 1 receptors are located on _______ synaptic membranes in the heart.
  • Stimulation activates ________, which converts ATP to cAMP.
  • Increases heartrate, conduction and contractility.
  • “Positive ______”
  • Chronotropy, dromotropy (affects the conduction speed in the AV node), inotropy
A
  • post
  • adenylyl cyclase
  • inotrope
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25
Q

Beta 2 Receptors

  • Located on post synaptic receptors in ______ and _______.
  • Stimulation _____ smooth muscle, resulting in bronchodilation, vasodilatation, and relaxation of the _____,______, and ______..
A
  • smooth muscle and gland cells.
  • relaxes
  • uterus, bladder and gut
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26
Q

Familiar Drugs and Classifications

Alpha nonspecific agonist:
* ____
* ____

Alpha 1 agonist specific:
* ________
* ______

Alpha 2 agonist selective:
* _____
* _____

A
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27
Q

Familiar Drugs and Classifications

Alpha nonspecific antagonist:
* ____
* ____

Alpha 1 antagonist selective:
* ________
* ______

Alpha 2 antagonist selective:
* _____
* _____

A
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28
Q

Catecholamines

  • Stimulate adrenergic receptors
  • Endogenous catecholamines include:
  • Non-endogenous (or synthetic sympathomimetic) catecholamines include _____ and _______.
A
  • dopamine, norepinephrine, and epinephrine.
  • isoproterenol and dobutamine
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29
Q

Epinephrine

  1. Stimulates ____,_____,____,____ receptors
  2. Alpha 1 stimulation increases _____ and _____ pressures and systolic BP. However, stimulation of alpha 1 receptors in the skin, mucosa, and hepatorenal vasculature causes vasoconstriction and decrease flow.
  3. Beta 1 stimulation causes increase in contractility & heart rate, which leads to increased ______ and ________.
  4. Beta 2 stimulation causes vasodilation in ________ and bronchial smooth muscle; may decrease ______ pressure.
  5. ___________ potentiate dysrhythmic effects.
A
  1. Alpha 1 + 2, Beta 1 + 2
  2. coronary and cerebral perfusion
  3. CO and MVO2 (demand)
  4. skeletal muscles; diastolic
  5. Volatile anesthetics
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30
Q

Epinephrine

  1. Principal pharmacologic treatment for _______ and _______.
  2. Complications include:.
  3. Dosage: ___-___ mg depending on cardiac compromise
  4. Cardiac Surgery :
  5. Available as an infusion of _________ @ _______mcg/min
  6. Administer 1 mg Q 3min in pulseless arrest
  7. Titrate to effect
A
  1. anaphylaxis and ventricular fibrillation
  2. cerebral hemorrhage, coronary ischemia, and ventricular arrhythmias
  3. 0.05 -1
  4. 0.01-0.05 mcg/kg/min
  5. 1 - 2mg/250ml; 2 – 20
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31
Q

Norepinephrine

  1. Endogenous neurotransmitter for alpha and beta receptors
  2. _________ Alpha 1 stimulation resulting in vasoconstriction, which increases systemic vascular resistance (both arterial and venous vessels) and may cause a ____________.
  3. Beta 1 agonist stimulation increase myocardial contractility.
  4. Beta 2 effects are minimal or absent
  5. Increased afterload and reflex bradycardia may prevent an increase in ________.
  6. Increased ___________ limits usefulness in cases of refractory shock.
  7. Decreases _______ blood flow
  8. Available in 4 or 8 or 16 mg in 250ml infusion
  9. Initiate at _______; titrate up to _____ mcg/min (non-weight based?) to effect
  10. Cardiac surgery ______-_____ mcg/kg/min
A

2 - Direct; reflex bradycardia.

5 - cardiac output.

6 - myocardial oxygen demands

7 - renal

9 - 2 – 4 mcg/min; 20

10 - 0.01-0.05

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32
Q

Dopamine

  1. Effect is dose-dependent
  2. Nonselective _____ and _____ adrenergic agonist effects
  3. Directly stimulates ____, ______, and ______ receptors
  4. Unique because it stimulates dopamine (dopaminergic) receptors and increases ______ blood flow and, thus, ________.
  5. Available as an infusion _____mg/____ml
A
  1. direct and indirect
  2. dopamine, beta and alpha
  3. renal; diuresis
  4. 800 mg/250ml
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33
Q

Dopamine

  1. Renal vasodilation predominate at < _____mcg/kg/min.
  2. _______ stimulation at 2 – 10 mcg/kg/min resulting in increased myocardial contractility, HR and CO
  3. ________ stimulation at 10 – 20 mcg/kg/min resulting in increased PVR due to vasoconstriction.
  4. Doses > 20 mcg/kg/min and higher result in the release of _______, because dopamine is an intermediate product in the enzymatic pathway leading to the production of norepinephrine; thus acts __________ by releasing norepinephrine.
A
    • 2
  2. Beta 1
  3. Alpha 1
  4. norepinephrine; indirectly
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34
Q

Dopamine

  • High doses can inhibit _______ and cause _______.
  • ________ metabolism
  • Extravasation can cause intense vasoconstriction – consider using _______ to prevent tissue extravasation injury.
A
  • insulin; hyperglycemia
  • Rapid
  • Phentolamine
35
Q

Dobutamine

  1. Synthetic catecholamine with structural characteristics of ___ and__.
  2. Acts on:
  3. Increases cardiac contractility (inotropic effects) – Most _______ properties as compared to epinephrine and norepinephrine.
  4. Dose-related increase in heartrate; increases myocardial oxygen demand
  5. Increases cerebral blood flow (CBF)
  6. Does not cause indirect release of _____.
  7. Decreases _____.
  8. Dosage :
A
  1. dopamine and isoproterenol
  2. Beta 1 receptors (selective beta 1 agonist)
  3. inotropic
  4. -
  5. norepinephrine
  6. systemic vascular resistance (beta 2 agonist)
  7. 2 – 20 mcg/kg/min
36
Q

Isoproterenol

  1. _______ catecholamine (pure beta agonist) with potent Beta 1 and Beta 2 effects
  2. Increased heart rate, myocardial contractility, _____ blood pressure
  3. No _______ effects.
  4. Excessive ______ and decreased ______ pressure may *decrease coronary flow *
  5. High incidence of :
  6. Infusion: ____mg/250ml @ ___-____
  7. Commonly used in :
A
  1. Synthetic
  2. systolic
  3. alpha
  4. tachycardia; diastolic
  5. cardiac dysrhythmias
  6. ** 2; 1 – 20 mcg/min
    **
  7. electrophysiology ablations
37
Q

Beta Agonists

  1. Relax ______ and ______ smooth muscles
  2. Used to treat _______
  3. In OB: used to stop ________
  4. Examples include :
A
  1. bronchioles and uterine
  2. bronchospasm
  3. uterine contraction
  4. Albuterol, Terbutaline and Ritodrine
38
Q

Sympathomimetics

  1. Synthetic drugs that are used as vasopressors to reverse hypotension.

Classified as
1. direct-acting:
1. indirect-acting:

A
  1. mimic the effects of norepinephrine
  2. evoke the release of endogenous norepinephrine
39
Q

Ephedrine

  1. Non-catecholamine; direct and indirect acting sympathomimetic
  2. Cardiovascular effects are similar to those of ________, although ephedrine is less potent with a ______ duration of action.
  3. Increases blood pressure by stimulating release of _______.
  4. Increases cardiac contractility and heartrate secondary to Beta 1 receptor stimulation.
A

1.-
2. epinephrine; longer
3. norepinephrine

40
Q

Ephedrine

  • Bronchodilator
  • Does not decrease ____ blood flow like the direct-acting Alpha 1 agonists
  • Dosage: ____-____mg bolus
  • Subsequent doses are increased secondary to depletion of norepinephrine
  • Available 50mg in 1 ml
  • Dilute with 9 ml NS to create 5 mg/ml in a 10 ml syringe
A
  • uterine
  • 2.5 - 10
41
Q

Phenylephrine

  1. Non-catecholamine, ______ acting (mimics the effects of ______) Alpha 1 agonist
  2. Primary effect is peripheral vasoconstriction, which increases systemic vascular resistance and BP
  3. No _______ effects
  4. Reflex ________
  5. Decreases _______ blood flow
  6. Increases cerebral blood flow
  7. Available as 10 mg in 1ml
  8. 10 mg mixed in 250 ml = 40 mcg/ml
  9. Infusion rate: ____-____ mcg/kg/min
A
  1. direct; norepinephrine
  2. -
  3. beta
  4. bradycardia
  5. renal

  1. 0.25 – 1
42
Q

Phenoxybenzamine

  1. ______Alpha antagonist
  2. Blockage at Alpha ____ is greater than Alpha ____.

Used primarily for:

A
  1. Non-selective
  2. 1; 2

  1. Chronic medical control of patients with pheochromocytoma
  2. Raynaud’s disease by reversing vasoconstriction in the hands
43
Q

Phentolamine (Regitine)

  1. _______ alpha antagonist: smooth muscle relaxation, which leads to peripheral vasodilation, decreased BP (alpha 1) and reflex ______ (alpha 2).
  2. Reflex tachycardia & ________.
  3. Dosage: ___-____mg bolus
  4. Used to treat:__________ , ___-____ mg locally infiltrated to prevent tissue necrosis
A
  1. Competitive; tachycardia
  2. postural hypotension
  3. 1 – 5
  4. extravasation of alpha agonist; 5 – 10
44
Q

Prazosin (Minipress)

  1. ______receptor antagonist
  2. Dilates both arterioles and veins
  3. Decreases ____ and _____.
  4. Virtually no _______ secondary to lack of alpha 2 antagonistic
  5. *______ is effective for BPH and HTN
  6. *_______ is for BPH only but may cause orthostatic hypotension.
A
  1. Alpha 1
  2. -
  3. SVR and Preload
  4. tachycardia
  5. Doxazosin
  6. Tamsulosin
45
Q

Clonidine (Catapress)

  1. Central acting on Alpha 2 agonist receptors located in the ________ of the spinal cord
  2. Decreases outflow of the sympathetic nervous system by reducing plasma catecholamine levels
  3. Negative chronotropic effects; decreases _____, ______, and _____.
  4. Sedative and analgesic effects _______ anesthesia requirements.
  5. Effective in suppressing the signs and symptoms of ________ from opioids
  6. Adverse effect is ________ when abruptly discontinued
  7. Transdermal __-___ mg/released QD
  8. Intrathecal ___-___ mcg
  9. Intravenous ___-___ mcg/kg
  10. PO ___-___ mcg/kg
A
  1. dorsal horn
  2. -
  3. CO, SVR and BP
  4. decrease
  5. withdrawal
  6. rebound HTN
  7. 0.1 - 0.3
  8. 75 – 150
  9. 1 – 3
  10. 3 – 5
46
Q

Dexmedetomidine (Precedex)

  1. Greater affinity for the alpha 2 receptor, than clonidine (______:1 alpha 2 )
  2. _______ effects
  3. Sympathetic outflow is reduced
  4. Minimal respiratory depression; may see hypotension and bradycardia
  5. Loading dose of ___-___ mcg/kg over 10 minutes
  6. Followed by infusion (___-___ mcg/kg/hr)
A
  1. 1600
  2. Sympatholytic

  1. 0.5 – 2
  2. 0.2 – 0.7
47
Q

Yohimbine

  1. ____-synaptic ______-adrenergic antagonist
  2. ______ sympathetic nervous system activity, and can result in increasing the amounts of _____ and ________ in the blood stream
  3. Increases _____ and ______.
  4. Used as a _______ supplement and to increase ______
  5. “Point and shoot” – parasympathetic and sympathetic- erection and ejaculation
A
  1. Pre- ; alpha-2
  2. Increases; epinephrine and norepinephrine
  3. blood pressure and heart rate
  4. weight loss; libido
48
Q

Beta Antagonists (Blockers)

  1. Blocks the effects of catecholamines on the ____ and ______.
  2. β-Blockers produce important anti-ischemic effects and are a first-line therapy for patients with: (4)
  3. Blockers bind to β1-adrenoceptors and inhibit the actions of circulating catecholamines and norepinephrine released from _________ sympathetic neurons.
A
  1. heart and lungs.
      • ST- and non–ST-segment elevation,
      • myocardial infarction in the absence of cardiogenic shock,
      • hemodynamically significant bradyarrhythmias, or
      • reactive airway disease.
        3 - postganglionic
49
Q

Beta Antagonists (Blockers)

  1. The decrease in heart rate produced by β-blockers prolongs ______, increases coronary blood flow to the ______, enhances coronary collateral perfusion to ischemic myocardium, and improves oxygen delivery to the coronary microcirculation.
  2. These combined effects serve to reduce myocardial oxygen demand while simultaneously increasing ______.
  3. β-Blockers have also been shown to inhibit ________.
A
  1. diastole, LV
  2. supply
  3. platelet aggregation.
50
Q

Inderal (Propranolol)

  1. ________ Beta 1 and Beta 2 antagonist (Beta ___ > Beta ____) – prototypical B-Blocker (“gold standard”).
  2. Decreases HR and CO, which decreases myocardial oxygen requirements
  3. Decreases myocardial contractility
  4. Decreases spontaneous SA node firing; slows AV conduction; particularly effective in _________.
  5. Uses:
  6. Dosage: ______ mg IV in 0.5 mg increments Q 2 minutes

  1. Side effect:
A
  • Nonselective; B1> B2
  • slowing ventricular rate in SVT
  • Afib/Aflutter/SVT
  • 1 - 3

may cause bronchospasm

51
Q

Metoprolol (Lopressor)

  1. _________ antagonist
  2. Action: Decreases HR and CO
  3. Cardioprotective
  4. Uses:
  5. Dosage: ______ mg IV - given in 5 mg increments Q 2 - 3 minutes
  6. Elimination half life: 3-4 hours
A
    1. Selective Beta 1
    1. Afib/Aflutter, HTN, SVT
    1. 5
52
Q

Atenolol / Tenormin

  1. _________ antagonist
  2. Similar to metoprolol in that it is relatively ______.
  3. The lack of _______ results in a more predictable blood level following oral dosing
  4. Use: Mostly PO for _______ – long acting
  5. Dosage: ___ mg IV over 10 minutes
  6. ____ mg PO QD – primary advantage once a day
A
  1. Beta 1 selective
  2. cardioselective
  3. first pass metabolism
  4. HTN
  5. 5mg
  6. 50
53
Q

Esmolol (Brevibloc)

  1. _______ antagonist, ultra-short acting
  2. Action: Decreases _____ and _____
  3. Dosage: 10 mg IVP
  4. Infusion: Load with _____mcg/kg over 5 minutes f/b ___-___ mcg/kg/min
  5. Metabolism: ______ and ______ to inactive metabolites. The half life is ~9 minutes.
A
  1. Selective Beta 1
  2. HR and CO
    3.-
  3. 250; 25 – 50
  4. hydrolysis by RBC’s and plasma esterases
54
Q

Mixed Alpha and Beta antagonists

Labetalol (Trandate)

  1. Action: Blocks
  2. Ratio of alpha to beta blockage is:
  3. Decreases ____, _____, and _____.
  4. CO slightly depressed or unchanged
  5. Lowers BP ______ reflexive increase in HR*
  6. Use with caution in patients with:
  7. Dosage: _____-____mg/kg IV
  8. Half life 3 - 8 hours
A
  1. Alpha 1, Beta 1 and Beta 2
  2. 1:7* (IV)
  3. PVR, BP and HR
  4. -
  5. without
  6. reactive a/w
  7. 0.1 - 0.5
55
Q

Timolol (Blocadren)

  1. Mostly used to:
  2. ________ beta blocker
  3. Used in the treatment of ______.
A
  1. decrease IOP by decreasing formation of aqueous humor
  2. Non-selective
  3. glaucoma
56
Q

Phosphodiesterase Inhibitors

  1. Alters intracellular Ca2+regulation to enhance __________ without affecting catecholamine release or activation of beta1-adrenoceptors
  2. PDE III inhibitors cause pronounced arterial and venous ________ by blocking _________ and facilitating the actions of this second messenger in vascular smooth muscle.
  3. Intravenous or inhalational administration of PDE III inhibitors also reduces ___________.
  4. The use of PDE III inhibitors is contraindicated for the treatment of _________, however these drugs continue to be of central importance for the treatment of _________ during cardiac surgery and in the intensive care unit

PDE Inhibitors have pharmacologic properties approaching the characteristics of the ideal inotropic agent. They do not rely on stimulation of beta or alpha receptors and selectively inhibit phosphodiesterase III, the enzyme that breaks down cAMP. Increased levels of cAMP results in vasodilation, decreased PVR and promotes ventricular filling (i.e., increased ______).

Amrinone
Milrinone – currently, the most popular PDEI

A
  1. myocardial contractility
  2. vasodilation; cGMP-metabolism
  3. pulmonary vascular resistance
  4. chronic heart failure, acute LV dysfunction

preload

57
Q

Milrinone

  • Used extensively for _______ support during and after cardiac surgery
  • Milrinone enhances myocardial contractility and causes _____________, improving the likelihood of successful weaning of patients with poor LV function from cardiopulmonary bypass
A
  • inotropic
  • arterial and venous vasodilation
58
Q

Vasopressin

  1. Peptide hormone released from ______.
  2. Regulates ___________ in the kidney and exerts potent hemodynamic effects __________ of adrenoceptors
  3. Receptors (V1 [cell membrane of ___________],V2, & V3) are five-subunit helical membrane proteins coupled to _______.
  4. Activation of subtype triggers second messengers to increase __________.
  5. Effective for conditions where relative vasopressin deficiency exists: ex.:
A
  1. posterior pituitary
  2. water reabsorption; independent
  3. vascular smooth muscle; G proteins
  4. intracellular smooth muscle cell.
      • catecholamine-refractory hypotension,
      • vasodilatory shock,
      • sepsis,
      • cardiac arrest
59
Q

Vasopressin

Uses: (4)

Combined use with other vasoactive medications reduces overall dose of vasopressin

Sustained admin at higher doses may produce mesenteric ischemia, peripheral vascular insufficiency, and cardiac arrest

A
  1. Intraoperative hypotension due to ACEIs & ARBs refractory to admin of catecholamines or sympathomimetics
  2. Anaphylaxis
  3. Vasoplegia: severe hypotension after prolonged CPB
  4. Cardiac arrest resulting from Vfib, PEA, Asystole
60
Q

Nitroglycerin (NTG or Nitrate)

  • Relaxes ________
  • Venous dilatation predominates over arterial dilatation, which leads to decreased myocardial oxygen demand.
  • Decreases ______
  • Mechanism of action is similar to sodium nitroprusside (i.e., metabolism of ______)
A
  • vascular smooth muscle
  • preload
  • NO
61
Q

Nitroglycerin (NTG or Nitrate)

  1. Relieves myocardial ischemia by redistributing coronary blood flow to ischemic areas of the ________.
  2. May relieve _____________ spasm
  3. Rebound hypertension after discontinuation is less likely as compared to _______

  1. Available ___ - _____mg in 250ml glass bottle
  2. Infusion: ___-____mcg/kg/min
A
  1. subendocardium
  2. coronary artery
  3. Nipride

  1. 50 or 100
  2. 0.5 – 10
62
Q

Metabolism of NTG

  • Undergoes rapid reduction _______ in the liver and blood
  • One metabolic product is ______, which can convert hemoglobin (Fe+2) to methemoglobin (Fe+3)
  • Methemoglobinemia ______ occurs.

  • Treat with methylene blue __-___mg/kg over 5 minutes
A
  • hydrolysis
  • nitrate
  • rarely

1 - 2

63
Q

Sodium Nitroprusside (Nipride)

  1. Metabolism releases _______ - a naturally occurring potent vasodilator released by the ______.
  2. ________ relaxation –> dilation of arterial and venous vascular beds reduces both ______ and ______; increases CO resulting in decreased myocardial workload (reflex ________) and ischemia.
  3. Inhaled NO used to treat :
  4. Decreases BP by decreasing ______

  1. Available as _____ mg/250 ml
  2. Infusion ___-____mcg/kg/min
  3. Rapid onset within 1 - 2 minutes
  4. Protect infusion from sunlight
A
  1. nitric oxide; endothelial cells
  2. Vascular smooth muscle / preload and afterload/ tachycardia
  3. pulmonary hypertension
  4. SVR

  1. 50mg
  2. 0.5 – 10
64
Q

Sodium Nitroprusside (Nipride)

Vascular steal syndromes
* Coronary steal: shunts blood away from compromised coronary leading to worsening ischemia and infarction
* Cerebral steal: similar mechanism

Avoid in patients with ________ and _____.

Rebound hypertension can occur with sudden discontinuation

A

cerebral ischemia and increase in ICP

65
Q

Nipride metabolism

  1. Nipride enters ______ cells and receives an electron from the iron of oxyhemoglobin (Fe+2)
  2. This electron transfer results in an unstable nitroprusside radical and _____.
  3. Nitroprusside radicals decompose into ______ ions.
  4. Cyanide ions bind to tissue _______ which interferes with normal oxygen utilization and prevents oxygen from being released by the tissues.

Risk factors:

A
  1. red blood
  2. methemoglobin (Fe+3)
  3. cyanide
  4. cytochrome oxidase

  • malnutrition,
  • liver disease,
  • CPB and
  • hypothermia

Monitor for toxicity of metabolites:
Acid/Base balance & thiocyanate levels

66
Q

Acute Cyanide Toxicity

  1. Signs and symptoms (4):
  2. Mechanically ventilate with 100% oxygen

  1. Administer sodium thiosulfate _____mg/kg over 15 minutes
  2. Thiosulfate converts cyanide to ______, which is cleared via the _____.
A
  1. Metabolic acidosis
  2. Tachyphylaxis
  3. Increased mixed venous O2 (secondary to inability to metabolize O2)
  4. Also cardiac dysrhythmias

  1. 150
  2. thiocyanate; kidneys
67
Q

Hydralizine

  1. Relaxes _____ smooth muscle
  2. Decreases _______.
  3. Decreases BP
  4. Increases _____ and _____.
  5. Interferes with _______ utilization
  6. Used for intraoperative hypertension
  7. Administer 5 – 20 mg IV
  8. Onset 15 - 20 minutes; duration 2 - 4 hours.
  9. Elimination half life 4 h, but effective half life _______ h
A
  1. arteriolar
  2. systemic vascular resistance
  3. HR and CO
  4. calcium

  1. 100
68
Q

Calcium Channel Blockers (CCB)

  1. Selectively interfere with ______ ion movement across the cell membranes
  2. Decreases myocardial oxygen demand by decreasing:
  3. Cause small muscle relaxation and vasodilation
  4. Uses include treatment of HTN, SVT, coronary artery spasm, angina and cerebral artery vasospasm
A
  1. inward calcium
  2. afterload, contractility, HR, and conduction through the AV node.
69
Q

Nifedipine (Procardia)

  1. Most ____ CCB
  2. ___ and ___ vasodilation
  3. Potential for ______ and ________.
  4. Uses: most specific application is for: (3)
  5. Dosage SL or PO: ___-____ mg
A
  1. potent
  2. Coronary and peripheral arterial
  3. hypotension and reflex tachycardia
  4. coronary vasospasm; HTN, angina

  1. 10-20
70
Q

Nicardipine (Cardene)**

  1. CCB; can be titrated IV
  2. Smooth muscle relaxation produces vasodilation of _______ and ______.
  3. Rapid onset; Half life 15 minutes
  4. Minimal cardiodepressant effects; does not decrease the rate of sinus node pacemaker or slow AV conduction
  5. Uses:

Available: 25mg in 250ml
Infuse 1 - 4 mcg/kg/min; titrate to achieve BP

A
  • peripheral and coronary arteries
  • HTN (Use cautiously in patients with acute ischemia.)
71
Q

Clevidipine

  1. Ultra-short-acting _______ Ca2+ channel antagonist
  2. Pronounced effects at the _______ resting membrane potentials typically in smooth muscle cells →highly selective for _____________; devoid of chronotropic or inotropic effects
  3. Good for patients with:
  4. Decreases SVR & ABP, no effect LV preload
  5. Metabolism by:
  6. Used for acute hypertension in cardiac surgery, pheochromocytoma, acute intracerebral hemorrhage, spinal surgery

Plasma half-life of ~2min

A
  1. dihydropyridine
  2. less negative; arterial vascular smooth muscle
  3. LV disfunction/AHF
  4. -
  5. plasma and tissue esterases
72
Q

Nimodipine (Nimotop)

  1. CCB; primary use is to prevent _________ following subarachnoid hemorrhage, which can occur ~4 – 14 days after initial event.
  2. Enters ______ and may block influx of calcium
  3. Now available only as an ______ medication; may be administered via NG tube
A
  1. cerebral artery vasospasm
  2. CNS;
  3. oral
73
Q

Diltiazem (Cardizem)

  • CCB; similar in chemical structure to verapamil
  • Selective ___________.
  • Uses:
  • _______ mg/kg IV slowly may repeat in 15 min Infusion: ___-____mg/hr
  • Half life 3-5 hours
A
  • coronary vasodilation
  • Angina, HTN, SVT, Afib, Aflutter
  • 0.25; 5-15
74
Q

Verapamil

  1. CCB; a derivative of ______.
  2. Depresses transmission of impulses via SA node and AV node by slowing HR and reducing contractility.
  3. Do not use in_____ or _________ as it inhibits the intrinsic conduction pathway.
  4. Use with caution in patients who are:
  5. Uses:
  6. Dosage: ____mg IV
A
  1. papaverine
  3. WPW or other ventricular dysfunction conduction abnormalities
  4. beta-blocked.
  5. SVT, Afib, Aflutter, chronic HTN
  6. 5
75
Q

ACE inhibitors

  1. Significantly reduced cardiovascular mortality for patients with ________.
  2. Block the conversion of ____ to _____ in the lungs
  3. Prevents ______ mediated vasoconstriction
  4. Examples:
  5. Uses:
  6. 20% of patients develop a :
A
  1. Heart Failure
  2. angiotensin I to angiotensin II
  3. angiotensin II
  4. Captopril, enalapril, lisinopril
  5. HTN, CRI, Chronic heart failure
  6. dry, chronic cough
76
Q

Angiotensin II Receptor Antagonists

  1. Increasing numbers of hypertensive patients being treated with ARBS are being scheduled for surgery.
  2. Hypotensive episodes occur more frequently after anesthetic induction in patients receiving ______ than other antihypertensive drugs and can be refractory to treatment with ephedrine and phenylephrine.
A

ARBS

77
Q

ARBS: Angiotensin II Receptor Antagonists

A
  • Candesarten (Atacand)
  • Eprosarten (Teveten)
  • Irbesarten (Avapro)
  • Losarten (Cozaar)
  • Olmesarten (Benicar)
  • Telmisartan (Micardis)
  • Valsartan (Diovan)
78
Q

ARBS Combination Products

A
79
Q

Antiarrhythmic Agents

Critical treatment steps before administration of any antiarrhythmic agent:

A
  • Manage electrolyte abnormalities
  • Treat underlying disease processes – i.e., myocardial ischemia
  • Beta Adrenergic receptor antagonists are very effective but often underused in the perioperative period.
  • Many arrhythmias are adrenergically-mediated, versus vagally-mediated.
80
Q

Class I: ___________

  • Common property of inhibiting the fast inward _______ current carried by the sodium ion; subgroups based on the diversity of other effects.

*Class IA

*Class IB

*Class IC

A

Sodium Channel Blockers

  • depolarizing
81
Q

Class II:

Very effective antiarrhythmics in patients during the perioperative period, or patients who are critically ill, primarily because they are ______-mediated.

Examples:

A

Beta Adrenergic Antagonists

adrenergically

Propanolol
Metoprolol
Esmolol

82
Q

Class III:

Agents that block potassium channels, thereby prolonging ________.

Examples:

A

Potassium Channel Blockers

repolarization

Amiodarone
Bretylium
Sotalol (also has Class II Beta adrenergic blocking activity)

83
Q

Class IV:

Calcium channel antagonistspreventcalciumfrom entering cells of the heart and blood vessel walls, resulting in _____________.

Also calledcalcium channel blockers, they relax and widen blood vessels by affecting the muscle cells in the arterial walls.

Examples:

A

Calcium Channel Antagonists
- lower blood pressure

Verapamil
Nifedipine
Diltiazem

84
Q

Other antiarrhythmic agents:

  1. Digoxin – digitalis glycoside for _____ and to control _____.
  2. Adenosine – endogenous nucleotide
  3. Potassium – to maintain electrolyte balance
  4. Magnesium
A
  1. CHF; supraventricular cardiac dysrhythmias

CVT (6 decks)

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