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CV Pharm > Midterm > Flashcards

Midterm Flashcards

1
Q

List 5 variables affecting anesthesia induction drug dose selection

A

Based on weight (mg/kg)
Individual drug dose based on use of adjuvant anesthesia drugs
Elderly require less, young require more
Trauma/Shock require less
Poor heart function require less
Drug dose selection may be variable depending on timing

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2
Q

List 6 factors which may affect the hemodynamic response to induction agents

A 
Premedication
Dose of drug
Speed of drug administration
CV disease and compensation
EF 
Emotional state
Baseline autonomic tone
Home medications
Influence of adjuvant anesthesia drugs
Age 
Diabetes
Hypertension history
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3
Q

Describe the hemodynamic effect(s) associated with the use of propofol,

A

effects vary depending on whether bolus or infusion, most profound effect is a decrease in BP, greater than any other agent, alters baroreceptors (decreases reflex increase in HR), decreases preload, contractility and afterload (CO, SV), vasodilates d/t: decrease in sympathetic outflow, inhibits sympathetic vasoconstrictor activity) also direct vasodilation (either decreased Ca mobilization or increased N2O production)

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4
Q

Describe the hemodynamic effect(s) associated with the use of thiopental

A

: Increase HR, Decrease CI, BP (15-20% decrease with 20-25% increase in HR due to baroreflex from venous pooling), decrease V filling by venous pooling (depression of medullary vasomotor center), histamine is high (>6mg/kg) doses, decreased sympathetic outflow, decrease in contractility d/t decrease in available Ca to myofibrils, in the absence of an adequate baroreflex response (e.g. Hypovolemia, CHF, beta blockade) CO and BP fall dramatically d/t uncompensated peripheral pooling and direct myocardial depression

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5
Q

Describe the hemodynamic effect(s) associated with the use of Methohexital

A

increases HR, no change vs decrease in CI, decrease in BP, profound in HTN, decreased V filling, from venous pooling, decreased sympathetic outflow, minimal hemodynamic effect in healthy and when administered slowly, decrease in contractility due to decrease in available calcium to myofibrils, in absence of adequate baroreflex response (e. G. Hypovolemia, CHF, beta blockade) CO and BP fall dramatically due to uncompensated peripheral pooling and direct myocardial depression, same as STP?

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6
Q

Describe the hemodynamic effect(s) associated with the use of etomidate

A

considered to be drug that changes hemodynamic variables least, paradigm is that “if 10 mg etomidate and 100mcg fentanyl kills them they won’t live anyway”, BP and contractility are minimally affected in patients with CHF (however, SBP decreases 20% with VHD, max decrease in blood pressure in all studies is 19% d/t 10-15% decrease in SVR, effects not significantly altered by adjuvant drugs, very useful in hypovolemic patients, doses > 0.45mg/kg associated with decreased SVR, decreased CI

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7
Q

Describe the hemodynamic effect(s) associated with the use of ketamine

A

most prominent effects at doses > 1mg/kg include significant increase in HR, CI and SVR, MVO2 is increased dramatically, increases PVR > SVR, hemodynamic depression of ketamine more pronounced when inhalation used, ketamine enhances dysrhythmogenic effects of epinephrine, indirect hemodynamic effects mimick ephedrine such that second dose less than first, and may not have same effect if catecholamines depleted (tamponade, critically ill), direct negative inotropic effect but SNS activation override this effect, combine ketamine and benzo very stable hemodynamically (effects blunted by benzo)

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8
Q

List three benefits of using nitrous oxide in addition to the potent inhaled anesthetics

A

MAC 106% (not useful as sole anesthetic), no decrease in BP when used alone but will decrease when other drugs used, can be used to hasten onset of more potent gases, ultrashort duration, useful to decrease dose of longer lasting gases

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9
Q

List four potential indications for induction with inhalation anesthetics such as sevoflurane instead of IV agents

A

Patients with compromised airway, (polyps, tumor, tracheal stenosis), children whose lack of cooperation makes it difficult to place IV, patients with indwelling endotracheal tube or tracheostomy, patients with needle phobia, induction usually accomplished IV

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10
Q

Describe dosing of hypnotics, commonly used for cardiac anesthesia

A

Hypnotics:
Propofol: 0.2-1.5mg/kg
Thiopental: 0.5-4mg/kg
Etomidate: 0.1-0.3mg/kg

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11
Q

Describe dosing of opioids commonly used for cardiac anesthesia

A

Opioids:
Fentanyl: 3-25mcg/kg
Sufentanil: 0.5-2mcg/kg
Remifentanil: 0.1-0.75mcg/kg/min

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12
Q

Describe dosing of muscle relaxants commonly used for cardiac anesthesia

A 
Muscle Relaxants: 
	Cisatracurium: 70-100mcg/kg
	Vecuronium: 70-100mcg/kg
	Pancuronium: 70-100mcg/kg
	Succinylcholine: 1-2mg/kg
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13
Q

Describe the primary mechanism thought to be responsible for cardiovascular effects of the volatile anesthetics

A

ISO , des, and sevo reduce intracellular calcium concentration in cardiac and vascular smooth muscle
Mechanism is though to involve a reduction in calcium influx through the sarcolemma and a depression of calcium release from the sarcoplasmic reticulum
End result is a depression

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14
Q

Describe the relationship between dose of iso, des, and sevo on blood pressure, SVR, heart rate and cardiac index

A

Effect on Blood Pressure: all agents decrease blood pressure in dose related fashion, mainly due to a decrease in SVR, CI is usually maintained though mildly depressed
Effect on SVR: all potent agents decrease SVR in dose related fashion, effects of newer agents differ from halothane (halothane decrease CI with minimal effect on SVR)
Effect on CI: Stroke volume decreases dust to vasodilation and preload reductions, but HR increases and is compensatory such that cardiac index is reasonably sustained.
Effect on HR: HR level is increased and CO is sustained at near awake values at all levels of desflurane anesthesia, HR also increases with sevo but only with greater MAC values, alterations in HR are a result of modulation of SA node automaticity modulation of baroreceptor reflex activity and SNS activation

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15
Q

Compare HR changes with the use of desflurane, sevoflurane, and isoflurane

A

HR level is increase and CO is sustained at near awake values at all levels with DESFLURANE
HR increases but only with greater MAC values with SEVOFLURANE
Alterations in HR are a result of modulation of SA node automaticity modulation of baroreceptor reflex activity and SNS activations
HR stays relatively the same with ISOFLURANE

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16
Q

Describe the effect of N2O and modest doses of fentanyl on MACBAR of sevoflurane and desflurane

A

MAC BAR for incision is 1.3 MAC for desflurane and isoflurane + 60% N2O
MACBAR for sevoflurane is 2.2 MAC + 60% N2O
The addition of 1.5-3mcg/kg fentanyl decreases incision MACBAR to 0.4 MAC
Tracheal intubation is similar to skin incision

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17
Q

Describe the effects of the three modern volatile agents on conduction, contractility, dysrhythmia potential, baroreflexes the ischemic heart

A

All three agents depress myocardial contractility and blood pressure
All three agents prolong AV nodal conduction and QT interval
All three predispose to catecholamine induced dysrhythmias, potent inhaled anesthetics attenuate barorefleses in dose related fashion
Sevoflurane may depress HPV the least

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18
Q

Describe the effect of left ventricular dysfunction on the circulatory effects associated with the volatile agents

A

Desflurane and isoflurane exert mild beneficial actions on LV function during MI by restoring isovolumic relaxation and enhanced filling
ISO has been shown to enhance recovery of post ischemic, reperfused (stunned) myocardium
Desflurane exerts same effect on dogs?
All potent agents mimic ischemia preconditioning, protecting against further ischemia

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19
Q

Describe the effects of the volatile agents on coronary blood flow

A

All potent agents decreasecoronary vascular resistance but coronary blood flow decreases due to effects on diastolic blood pressure
Ratio of flow between epicardium and endocardium is sustained
Coronary steal has been postulated, especially with isoflurane but usually ischemia is due to hypotension
No steam phenomenon has been found in studies when BP controlled

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20
Q

Identify the volatile considered to be the agent of choice for patients with cerebrovascular disease undergoing cardiac surgery

A

Isoflurane is the agent of choice

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21
Q

List three non anesthetic drugs considered to have a synergistic relationship with volatile agents on hemodynamics

A

Depressant drugs add to the depression from inhaled agents
Prodysrhythmic drugs that cause dysrhythmias are no more likely in general to cause more dysrhythmias
Larger dose of Isoproterenol is required to increase HR
Limited interaction with CBD’s but may be synergistic with ACE inhibitors and to a lesser degree beta blockers

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22
Q

Describe how adjuvant anesthetic agents may interact with volatile agents to affect hemodynamics

A

N2O significantly decreases cardiac output and SV bur decreases MAC requirements
Fentanyl decreases MAC along with systemic vascular resistance and HR with all agents
Propofol causes dose related circulatory depression (decreased cardiac output and blood pressure)
Dexmedetomidine modestly affects circulatory effects (decreased HR and systemic vascular resistance)

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23
Q

Describe the circulatory effects of N2O and how it is affected by the use of other anesthetic agents

A

Activated the SNS and increases SVR
Activation of SNS leads to increase in CVP and arterial pressure
Sympathetic response appears to be intact during co administration of volatile agents
In contrast, when adm;II steered with opioids the addition of N2O augments cardiac depression

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24
Q

Describe the effect of moderate to high dose opioids on hemodynamics

A

More significant bradycardia and vasodilation are seen at greater doses or when combined with other anesthesia drugs

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25
Q

Discuss possible mechanisms for hemodynamic effect of the opioids

A

Prelaod and afterload are reduced by opiod induced depression of vasomotor centers in the medulla and decreased sympathetic tone
Most of the hemodynamic effects of opioids can be related to their influence on sympathetic outflow from CNS
Mild parasympathomimetic effect in cardiac cells not considered clinically significant
Bradycardia is produced by a direct stimulant effect on the central vagal nuclei, vagal it ic drugs reverse this (atropine, glycopyrrolate)

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26
Q

Identify the opioid considered to have most favorable effect on HR and BP for intubation and intraoperative BP control

A

Sufentanil

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27
Q

Compare the effect of fentanyl and sufentanil on on epinephrine and NE levels

A

Lower post op NE levels with sufentanil including fentanyl
More consistent epinephrine levels with sufentanil especially post extubation
Lower intraoperative epinephrine levels with Demerol than other opioids

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28
Q

List 5 effects of cardiopulmonary bypass on anesthesia drug disposition

A 
Hemodilution
Organ blood flow
Hypothermia
Protein binding: heparin, adjuvant drugs
Sequestration in the lungs
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29
Q
  1. Discuss the determinants of blood pressure
A
  • Blood pressure is COX Peripheral Vascular Resistance
  • CO is HR X SV
  • SV is Preload X Contractility X Afterload
  • Afterload is impedance to injection/ pressure required to open valve/ CO X
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30
Q
  1. Discuss the determinants of cardiac output
A
  • HR and Stroke Volume
  • Stroke Volume= Preload, Afterload, and Contractility
  • HR dependent on SNS/PSNS/SA node firing
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31
Q
  1. Discuss the determinants of systemic vascular resistance
A
  • SVR= Tone X Viscosity
  • Tone dependent on Radius, Pressure Gradient, Vessel length
  • Viscosity dependent on COP and Hgb
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32
Q
  1. Describe the hemodynamic effects of alpha, beta, dopaminergic and muscarinic receptors
A
  • Alpha 1 vasoconstriction
  • Alpha 2 blocks output/ vasodilates
  • Beta 1 increases HR and contractility
  • Beta 2. Vasodilates and increases gluconeogenesis
  • Dopamine has a variety of responses depending on the dose
  • Muscarinic decreases HR and activates salivary/sweat glands and to a much lesser degree decreases vascular tone
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33
Q
  1. Describe the hemodynamic effects of alpha, beta, dopaminergic and muscarinic receptors
A
  • Sympathetic pathway
    o Preganglionic nerves release acetylcholine as NT and considered “cholinergic”
    o Postganglionic NE as NT and are “adrenergic”
    o Adrenergic fibers can sustain output of NE during prolonged periods of stimulation
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34
Q
  1. Identify neurotransmitters at the preganglionic and postganglionic nerves in the sympathetic nervous system
A
  • Sympathetic pathway
    o Preganglionic nerves release acetylcholine as NT and considered “cholinergic”
    o Postganglionic NE as NT and are “adrenergic”
    o Adrenergic fibers can sustain output of NE during prolonged periods of stimulation
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35
Q
  1. Identify neurotransmitters at the preganglionic and postganglionic nerves in the parasympathetic nervous system
A
  • Parasympathetic pathway
    o Nerves of PNS leave CNS through CN III, V, VI, and X S2-S3
    o 75% of all PNS fibers are in the vagus nerve
    o All pre ganglionic nerves of SNS and PNS release acetylcholine as NT
    o Post ganglionic nerves of PNS are short and secrete acetylcholine as NT post ganglionic
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36
Q
  1. Describe how norepinephrine is removed from the nerve ending
A
  • Diffusion out of synaptic cleft and into circulation
  • Metabolized by O- Methytransferase (COMT) in synaptic cleft
  • Re-uptake into neuron, broken down by MAO
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37
Q
  1. Describe the parasympathetic pathway and acetylcholine as a neurotransmitte
A
  • 75% of all PNS fibers are in the vagus nerve
  • All preganglionic nerves of SNS and PNS releases acetylcholine as the NT
  • Postganglionic nerves are short and secrete acetylcholine as the neurotransmitter
  • Life of Acetylcholine
    o Synthesized from two precursors (choline and acetylcoenzyme A)
    o Stored in vesicles and released in response to action potential
    o Following release binds to receptors (nicotinic or muscarinic) on postsynaptic cell
    o Upon dissociating from receptor immediately broken down by acetylcholinesterase into acetate and choline
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38
Q

List the muscarinic subtypes which are inhibitory

A
  • Eye: contraction of ciliary muscle for near vision
  • Heart: decreased rate
  • Lung: constriction of bronchi, increased secretions
  • Bladder: relaxation of bladder, increased bladder pressure
  • GI Tract: salivation, defecation
  • Sweat glands: sweating
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39
Q

List 4 mechanisms of adrenergic receptor activation

A
  • Adrenergic agonists produce three effects by activating adrenergic receptors (sympathomimetics)
  • Adrenergic agonists have a broad range of indications ranging from heart failure to preterm labor
  • Drugs can activate receptors by four basic mechanisms (direct receptor binding, promotion of NE release, blockade of NE reuptake, and inhibition of NE inactivation)
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40
Q

List three catecholamine adrenergic agonists

A

Catecholamines

  • Contain a catechol and amine group
  • Common properties include no available oral form, brief duration of action, cannot cross BBB
  • Examples include: epinephrine, norepinephrine, isoproterenol, dopamine and dobutamine
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41
Q

List three non catecholamine adrenergic agonists

A

Non Catecholamines

  • Have an amine group of a catechol group
  • Lack catechol group noncatecholamines are not substrates for COMT and are metabolized slowly by MAO inhibitors
  • May be administered orally as they do not undergo rapid metabolism by COMT, able to cross BBB
  • Examples include: ephedrine, phenylephrine, and terbutaline
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42
Q

List three cardiovascular effects of beta 1 receptor activation

A
  • Increased HR
  • Increased contractility
  • Increased automaticity
  • Increased conduction through AV node
  • Renin release from juxtalomerular cells
  • Viscous, amylase filled secretions from salivary glands
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43
Q

Describe cardiopulmonary and vascular effects of PDE- 3 inhibitors

A
  • Cyclic AMP is broken down by an enzyme called cAMP dependent phosphodiesterase (PDE)
  • Isoform of this enzyme that is targeted by currently used clinical drugs is the type 3 form (PDE 3)
  • Inhibition of this enzyme prevents cAMP breakdown and thereby increases its intracellular concentration increasing
    o Cardiac inotropy
    o Chronotropy
    o Dromotropy
  • Systemic circulation
    o Vasodilation
    o Increased organ perfusion
    o Decreased SVR
    o Decreased arterial BP
  • Cardiopulmonary
    o Increased contractility
    o Increased HR
    o Increased SV and EF
    o Decreased preload
    o Decreased PCWP
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44
Q

Describe the different effects of different dopamine doses

A
  • Induces natriuresis in dose range of 1-5mcg/kg/min
  • At this dose dopamine binds with the D1 receptor, dilating renal and messenger ic blood vessels
  • At 5-10 mcg/kg/min primarily beta 1 with increases in contractility and HR
  • > 10 mcg/kg/min primarily alpha 1
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45
Q

List three uses of vasopressin

A
  • Vasopressin, hormone found in hypothalamus primarily used in body to handle renal regulation of volume
  • Also potent vasoconstrictor (V1 receptor) works both in kidneys and blood vessels
  • Main non anesthesia uses are for treating volume losses in diabetes and bleeding esophageal varices
  • Useful for vasoplegia associated with infection and CPB
  • Some studies demonstrate renal, cerebral and pulmonary vasodilation while constricting systemic arterioles (including coronaries
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46
Q

Compare up and down regulation of adrenergic receptors

A
  • Up regulation( increased density of receptors) is seen with chronic decrease in receptor stimulation (seen with beta adrenergic antagonists)
  • Down regulation (decreased density of receptors) caused by chronic increase in receptor stimulation (beta adrenergic agonists as with inhaler
  • Receptor desensitization may occur with chronic exposure
  • Acidosis, hypoxia and drug interactions may also affect receptor activation
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47
Q

Describe the components of the skeleton of the heart

A

o Skeletal base
1. Valve annuli
2. Aortic and pulmonary roots
3. Central fibrous body
4. Fibrous trigones
o Atria and ventricular chamber arise separately
o Contraction of muscle fibers creates “twisting” motion

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48
Q

Compare wall thickness of the RV and LV

A

o Walls of RV are only 4-5 mm

o LV wall thickness is 8-15 mm thick

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49
Q

Identify the location of the coronary sinus

A

o Coronary sinus is located between AV orifice and valve of IVC

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50
Q

Compare the upper third of the septum to the lower two-thirds in regard to histology

A

o Both RV and LV have papillary muscle which attach to chordae tendinae
o Upper third of septum is smooth endocardium, lower 2/3 is trabeculae
o Myocardium has three layers, middle is muscular which runs in spiral fashion

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51
Q

Identify the coronary artery which typically provides flow to the bundle branches. MV papillary muscles and SA/AV nodes

A

o LAD provides flow to anterior 2/3 of interventricular septum (IVS), R/L bundle branches, MV papillary muscles, anterior-lateral and apical left ventricle
o CX provides flow to LA and posterior-lateral LV
o RCA provides flow to SA/AV nodes, RA, RV, posterior 1/3 of IVS

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52
Q

Identify the coronary artery which typically provides flow to the anterior, lateral, posterior and apical portions of the LV

A

o LAD provides flow to anterior-lateral and apical of LV

o CX provides flow to LA and posterior-lateral LV

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53
Q

Describe the effect of CAD on coronary vascular smooth muscle tone and anticoagulation

A

o Coronary endothelium modulates myocardial blood flow by relaxing or contracting underlying vascular smooth muscle
o Vascular endothelial cells express anticoagulant substances
o CAD adversely affect these autoregulatory functions

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54
Q

Definite coronary perfusion pressure and its components

A 
o	Perfusion Pressure
	CPP = DBP – LVEDP
	RV fills throughout cycle unless RV hypertrophy 
o	Myocardial extravascular compression 
	Worst in subendocardium 
	Lower heart rates minimizes compression 
o	Myocardial metabolism 
o	Neurohormonal control
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55
Q

Compare LV and RV perfusion in systole and diastole

A

o Blood flow is supplied by LAD, circumflex, and RCA
o Most blood flow to LV occurs DURING DIASTOLE due to diastolic pressure gradient
o Critical stenosis may affect contractility or conduction

o RV fills throughout cycle unless RV hypertrophy

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56
Q

Identify the portion of the myocardium most affected by extravascular compression and higher LVEDP

A

o Wall stress is typically greater in the subendocardium
 Blood supply is lowest due to LVEDP
 Demand is the highest

57
Q

Describe the key responses to CAD in the coronary circulation

A

o Coronary atherosclerosis is excessive accumulation of connective and smooth muscle cells, lipoproteins and minerals in the intima
o Arterial wall inflammation also present along with vasoconstriction
o Arterial obstruction “L” may be fixed or dynamic
o COLLATERAL FLOW AND REMODELING ARE KEY RESPONSES

58
Q

List two determinants of myocardial oxygen balance that both decrease supply and increase demand

A

o Heart rate

o PCWP

59
Q

Identify the distribution of the SNS responsible for increasing chronotropy and inotropy

A

o Increased SNS (T1-T4) increase chronotropy and inotropy (cardiac accelerate fibers)

60
Q

Describe the effect of increased parasympathetic activation on chronotropy

A

o SNS competes with PSNS (medulla) which decreases chronotropy and inotropy
o PSNS has only modest effect on inotropy (30%)

61
Q

Describe the role of accessory pathways in dysrhythmias

A

o Abnormal accessory pathways between the atria and ventricles may bypass the AV node and cause re-entrant dysrhythmias
o Purkinje network of fibers assure rapid distribution of depolarization

62
Q

Describe the normal impulse generation from the SA node to the Purkinje fibers

A

o Atrial depolarization (initiated in the SA node) is not indiscriminately transmitted throughout the heart
o AV node
o Bundle of His
o Purkinje fibers

63
Q

Identify and describe the basic contractile unite of the myocyte

A

o Sarcomere is the contractile unite of the myocyte consisting of “I” and “A” bands

64
Q

Discuss the role of calcium in contraction and its dispersal

A

o Sarcoplasmic reticulum surrounds contractile bundles and controls dispersal and reaccumulation of calcium

65
Q

Describe the effect of actin-myosin configuration on contractility (based on Frank-Staling Law)

A

o Contractile apparatus is composed of six major components
 Myosin, actin, tropomyosin, three-protein troponin complex
o Binding of myosin to actin stimulates a cascade of events causing contraction and relaxation

o Calcium-troponin C binding produces conformational change that expose the specific myosin-binding site
 Caused by 100 fold increase in intracellular calcium concentrations as occur during systole
 Sarcoplasmic reticulum removes calcium during diastole

o In contrast, cardiac muscles require calcium to contract
o Calcium ions bid to troponin and skeletal muscle (activated by Ca++)
o Coordinated contractions propel blood out of the ventricle

o Possess characteristics of both smooth muscle and skeletal muscle (ALL OR NONE, interconnected sarcomeres)
o Actn and myosin filaments interact for muscle contraction
o Resting sarcomere length determines contractility based on FRANK STARLING’S LAW

66
Q

Define LaPlace’s Law in relationship to wall tension/stress, potential energy, and LV thickness

A

o Wall stress and MVO2 varies directly with internal pressure and radius, and inversely with wall thickness
o Wall stress is typically greater in the subendocardium
 Blood supply is lowest due to LVEDP
 Demand is highest

o Contractility is determined by sarcomere/myocyte characteristics
o Myocyte length, potential energy and tension determined by Chamber volume/pressure, radius of chamber, and LV thickness

67
Q

Compare ion permeability (fast and slow channels in cardiac muscle in relationship to the ventricular muscle action potential

A

o Myocardial sarcomere not just contractile but able to conduct and generate an action potential
o Relatively permeable to sodium and calcium
o Ventricular muscle action potential has four phases from depolarization to repolarization

68
Q

Compare the SA node action potential to ventricular muscle action potential

A

o Each heart muscle has its own automaticity and rate (usually 35)
o SA node has its own automaticity and higher resting membrane potential (more permeable to sodium)
o NO phase 1 or 2
o AV node is second highest intrinsic rate

69
Q

Describe the events in the cardiac cycle in relationship to forward flow and valve opening/closing

A

o Synchronous depolarization of RV and LV initiates contraction
o Tricuspid and mitral valves close when ventricle pressure > atrial pressure
o Rapid ejection occurs when RV and LV pressures > pulmonary artery and aorta pressures
 Pulmonic and aortic valves open
 2/3 of end-diastolic volume ejected

70
Q

Define End-Systolic Pressure Volume Relationship (ESPVR) and its relationship to contractility

A

o ESPVR is heart rate INSENSITIVE index of contractility

71
Q

Define EDPVR and its relationship to ventricular compliance

A

o Increase in EDPVR (end-diastolic) denotes a reduction in LV compliance
o LV diastolic pressure is higher at each LV volume
o Simultaneous reductions in ESPVR and EDPVR often result with lower ejection fractions and HF

72
Q

Describe the effect of increasing PRELOAD on the PV loop, EDPVR, and stroke volume

A

o Preload increases shift the loop to the RIGHT
o Stroke volume increases
o Depending on the end-diastolic pressure-volume relationship (EDPVR) LV Pressure increases
 EDPVR is directly related to LV compliance

73
Q

Describe the effect of afterload on the PV loop stroke volume and ESPVR

A

o Afterload increases cause the loop to become NARROW and TALLER
o Lower stroke volumes and higher pressure results
o Higher end-diastolic volumes result
o ESPVR is reduced
 ESPVR is related to myocardial contractility

74
Q

Describe the effect of contractility on ESPVR, the PV loop and stroke volume

A

o ESPVR is heart rate insensitive index of contractility
o Affected by venous return and arterial vascular tone (preload and afterload)
o HF results in shift of LV volume to the right to compensate for decreased contractility
o Stroke volume is maintained at cost of pulmonary venous congestion

75
Q

List three ways the body compensates for heart failure

A
  1. Salt and water retention
     Augments preload via Frank-Starling effect
     Causes pulmonary congestion and edema
  2. Vasoconstriction
     Maintains BP for perfusion of vital organs
     Exacerbates pump dysfunction by increasing afterload and MVO2
  3. Sympathetic stimulation
     Increase hr and blood ejection
     Increases dysrhythmias, MVO2
76
Q

List CV and respiratory effects of the cardiovascular reflexes

A
  1. Valsalva maneuver -> Decrease hr, contractility, vasodilation
  2. Baroreceptor reflex -> Decreased hr, contractility, vasodilation
  3. Oculocardiac reflex -> bradycardia, asystole, dysrhythmias, hypotension
  4. Celiac reflex -> bradycardia, hypotension, apnea
  5. Bainbridge reflex -> increased hr, decreased BP, decreased SVR, diuresis
  6. Cushing reflex -> SNS resulting in hypertension
  7. Chemoreceptor reflex -> increased respiratory drive, increased BP
77
Q

Discuss the determinants of cardiac output

A

o Cardiac output dependent on stroke volume and heart rate
o Stroke volume dependent on preload, contractility, and afterload
o Heart grate dependent on SNS/PSNS/SA node firing

78
Q

Discuss the determinants of systemic vascular resistance

A

o SVR = tone X viscosity
o Tone dependent on radius, pressure gradient, vessel length (Poiseulle’s Law)
o Viscosity dependent on COP, Hgb

79
Q

Describe the hemodynamics effects of alpha, beta, dopaminergic and muscarinic receptors

A

o Alpha 1: vasoconstriction
o Alpha 2: vasodilation, blocks output
o Beta 1: increase heart rate and contractility
o Beta 2: vasodilation and increases gluconeogenesis
o Dopamine: has a variety of response depending on dose -> activates alpha 1, beta 1, dopamine receptors but NOT alpha 2 or beta 2 receptors; only activates dopamine receptors and dilates renal vessels

80
Q

Identify neurotransmitters at the preganglionic and postganglionic nerves in the sympathetic and parasympathetic nervous system

A
  1. Sympathetic
     Preganglionic nerves release acetylcholine as a neurotransmitter and considered “cholinergic”
     Postganglionic nerves release norepinephrine as neurotransmitter and are “adrenergic”
     Adrenergic fibers can sustain output of NE during prolonged period of stimulation
  2. Parasympathetic
     Preganglionic: acetylcholine
     Postganglionic nerves are short and secrete acetylcholine as the neurotransmitter
81
Q

Describe how norepinephrine is removed from the nerve ending

A

o Diffusion out of synaptic cleft and into circulation
o Metabolized by O-methytransferase (COMT) in syntactic cleft
o Re-uptake into neuron, broken down by monoamine oxidase (MAO)

82
Q

Discuss the receptor and hemodynamic effects of dexmedetomidine, carvedilol, norepinephrine, epinephrine, labetalol, esmolol

A
  1. Dexmedetomidine: alpha 2 agonists -> blocks reuptake of Norepinephrine; euphoria per
  2. Carvedilol: Mixed alpha/beta antagonists
  3. Norepinephrine: Non selective alpha agonists, beta 1 agonists
  4. Epinephrine: Non selective alpha, beta agonists
  5. Labetalol: mixed alpha/beta antagonists
  6. Esmolol: beta 1 antagonists
83
Q

Describe the parasympathetic pathway and acetylcholine as a neurotransmitter

A

o Nerves of PNS leave the CNS through CN III, V, VI, IX, and X, S2-S3
o 75% of all PNS fibers are in the vagus nerve
o All preganglionic nerves of SNS and PNS release acetylcholine as the neurtransmitter
o Postganglionic nerves are short and secrete acetylcholine as the neurotransmitter

o Acetylcholine synthesized from two precursors (choline and acetylcoenzyme A)
o Stored in vesicles and released in response to action potential
o Following release binds (nicotinic or muscarinic) on postsynaptic cell
o Upon dissociating from receptor immediately broken down by acetylcholinesterase into acetate and choline

84
Q

List the muscarinic subtypes which are inhibitor

A

o Allows a dramatic increase in drug selectivity (may influence neuromuscular junction without targeting PNS)
o By knowing what activation of each receptor subtype dose, we can predict the response of drugs specific for this receptor subtype

85
Q

List four mechanisms of adrenergic receptor activation

A

o Adrenergic agonists produce their effects by activating adrenergic receptors (sympathomimetics)
o Have a broad range of indications ranging from HF to pre-term labor)
o Activate by four basic mechanisms: direct receptor binding, promotion of NE release, blockade NE reuptake, and inhibition of NE activation)

86
Q

List three CV effects of beta-1 receptor activation

A

o Increased hr, contractility, automaticity, conduction through AV node
o Renin release from justaglomerular cells
o Viscous, amylase filled secretions from salivary glands

o Heart
 Tachycardia results from a Beta-1 mediated increase in the rate of phase 4 depolarization of SA node pacemaker
 Increased inotropy mediated by increased phosphorylation of Ca++ channels, including calcium channels in the sarcolemma and phospholamban in the SR
 Increase in AV node conduction velocity (Beta-1 stimulated increase in Ca entry increases the rate of depolarization of AV node cells)

o Kidneys
 Increased renin release by kidneys (Beta 1 receptors are present mainly on JTG cells, where receptor activation causes renin release

87
Q

Describe the cardiopulmonary and vascular effects of PDE-3 Inhibitors

A

o Cyclic-AMP is broken down by an enzyme called cAMP-dependent phosphodiesterase (PDE)
o Isoform of this enzyme that is targeted by currently used clinical drugs is the type 3 form (PDE3)
o Inhibition of this enzyme prevents cAMP breakdown and thereby increases its intracellular concentration by increasing cardiac inotropy, chronotropy, dromotropy

o Systemic: vasodilation, increased organ perfusion, decreased SVR, decreased arterial BP

o Cardiopulmonary: increased contractility, increased HR, increased SV/EF, decreased preload, decreased PCWP

88
Q

Describe the different effects of different dopamine doses

A

o 1-5 mcg/kg/min: dopaminergic -> binds to D1 receptor, dilating renal and mesenteric blood flow
o 5-10 mcg/kg/min: primarily beta 1 with increases contractility and hr
o > 10 mcg/kg/min: primarily alpha 1

89
Q

List three uses of vasopressin

A

o Hormone formed in the hypothalamus primarily used in body to handle renal regulation of volume
o Also potent vasoconstrictor (V1 receptor), works both kidneys and blood vessels
o Main nonanesthesia uses: treating volume losses in DM, bleeding in esophageal varies
o Useful for vasoplegia associated with infection and CPB
o Demonstrate renal, cerebral and pulmonary vasodilation while constricting systemic arterioles (including coronaries)

90
Q

Compare up and down regulation of adrenergic receptors

A

o Up regulation (increased density of receptors) is seen with chronic decrease in receptor stimulation (seen with beta adrenergic antagonists)
o Down regulation (decreased density of receptors) is caused by a chronic increase in receptor stimulation (beta adrenergic agonists as with inhaler)
o Receptor desensitization may occur with chronic exposure
o Acidosis, hypoxia and drug interactions may also affect receptor activation

91
Q

List five variables affecting anesthesia induction drug dose selection

A

o Usually based on weight (mg/kg)
o Individual drug doses based on use of adjuvant
o Elderly requires less, young require more
o Trauma/shock require less
o Poor heart function require less
o Drug dose selection may be variable depending on timing

92
Q

List six factors which may affect the hemodynamic response to induction agents

A 
o	Premedication 
o	Dose of Drug
o	Speed of drug administration
o	CV disease and compensation
o	Ejection Fraction
o	Emotional state
o	Baseline autonomic tone
o	Home medication
o	Influence of adjuvant drugs 
o	Age
o	Diabetes?
o	HTN history?
93
Q

Describe the hemodynamic effects associated with the use of propofol, thiopental, methohexital, etomidate, midazolam, and ketamine

A
  1. Propofol
    o Effects vary depending whether bolus or infusion
    o Most profound effects is a decrease in BP, possible greater than any agent
    o Altered baroreceptor activity decreases reflex increase in HR
    o Considered to decrease preload, contractility, and afterload (CO,SV)
    o Vasodilatory effect due to decrease in sympathetic outflow (inhibits sympathetic vasoconstrictor activity); direct vasodilation (either decreased calcium mobilization or increased nitric oxide production
94
Q

Describe mechanism responsible for blood pressure effects seen with the previously mentioned induction agents

A
  1. Propofol
    o Vasodilatory effect due to decrease in sympathetic outflow (inhibits sympathetic vasoconstrictor activity); direct vasodilation (either decrease calcium mobilization or increase nitric oxide production)
  2. Thiopental
    o Decrease in BP (15-20% decrease with 20-25% increase in HR due to baroreflex from venous pooling)
    o In absence of an adequate baroreflex response (eg, hypovolemia, CHF, beta blockade) CO and BP fall dramatically due to uncompensated peripheral pooling and direct myocardial depression
  3. Methohexital
    o In the absence of adequate baroreflex response (eg hypovolemia, CHF, beta blockade) CO and BP fall dramatically due to uncompensated peripheral pooling and direct myocardial depression
95
Q

List three benefits of using nitrous oxide in addition to the potent inhaled anesthetics

A

o MAC 106% not useful as the SOLE anesthetic
o No decrease in BP when used alone but will decrease when other drugs are used, as is usually the case
o Used to hasten onset of more potent gases
o Ultrashort duration
o Useful to decrease dose of longer lasting gases

96
Q

List four potential indications for induction with inhalation anesthetics such as Sevoflurane instead of IV agents

A

o Patients with compromised airway (polyps, tumor, tracheal stenosis)
o Children whose lack of cooperation makes it difficult to place IV
o Patients with indwelling ETT or tracheostomy
o Patients with needle phobia

97
Q

Describe effects associated with intubation after induction with etomidate, propofol, and midazolam

A
  1. Increase HR
  2. Increase SVI
  3. Increase CI
  4. Increase MAP
  5. Propofol and Midazolam decrease SVR, whereas Etomidate increase it
    * *can’t that one drug is better for cardiac surgery that the other, they all do same thing-just how you give them
98
Q

Describe the primary mechanism thought to be responsible for the CV effects of volatile anesthetics

A

o Isoflurane, desflurane and Sevoflurane reduce intracellular calcium concentrations in cardiac and vascular smooth muscle
o Mechanism is thought to involve a reduction in calcium influx through the sarcolemma and a depression of calcium release from the sarcoplasmic reticulum
o End result is a depression of the contractile state of the myocardium along with dilation of the peripheral vasculature

99
Q

Describe the relationship between dose of Isoflurane, Desflurane, and Sevoflurane on BP, SVR, heart rate, and CI

A

o All agents DECREASE BP in a dose-related fashion
o The decrease in BP with modern agents mainly due to a decrease SVR
o SV decrease due vasodilation and preload reduction, however hr increases and is compensatory such that CI is reasonably sustained
o CI is usually maintain though mildly depressed

100
Q

Compare heart rate changes with the use of Desflurane, Sevoflurane, and Isoflurane

A

o Heart level is increased and cardiac output is sustained at near-awake values at all levels of desflurane anesthesia
o Heart rate also increase with sevoflurane but only with greater MAC values
o Alterations in HR as a result of modulation of SA node automaticity, modulation of baroreceptor reflex activity, and SNS activation

101
Q

Describe the effect of Nitrous Oxide and modest doses of fentanyl on MACBAR of Sevoflurane and Desflurane

A

o MACBAR for incision is 1.3 MAC for desflurane and isoflurane + 60% Nitrous oxide
o MACBAR for sevoflurane is 2.2 MAC + 60% nitrous oxide
o The addition of 1.5-3 mcg/kg fentanyl decreases incision MACBAR to 0.4 MAC

102
Q

Describe the effects of the three modern volatile agents on conduction, contractility, dysrhythmia potential, baroreflexes and ischemic heart

A

o Depress myocardial contractility and blood pressure
o Prolong AV nodal conduction and QT interval
o Predispose to catecholamine-induced dysrhythmias
o Attenuate baroreflexes in a dose-related fashion

103
Q

Describe the effect of left ventricular dysfunction on the circulatory effects associated with the volatile agents

A

o Desflurane and isoflurane exert mild beneficial actions on LV function during myocardial ischemia by restoring isovolumic relaxation and enhanced filling

104
Q

Describe the effects of the volatile agents on coronary blood flow

A

o All potent agents decrease coronary vascular resistance but coronary blood flow decrease due to effects on diastolic blood pressure

105
Q

List three non-anesthetic drugs considered to have a synergistic relationship with volatile agents on hemodynamics

A

o Limited interaction with CBD’s but may be synergistic with ACE inhibitors and to a lesser degree beta blockers

106
Q

Describe how adjuvant anesthetic agents may interact with volatile agents to affect hemodynamics

A

o Nitrous oxide significantly decreases cardiac output and stroke volume but decreases MAC requirements
o Fentanyl decreases MAC along with systemic vascular resistance and heart rate with all agents
o Propofol causes a dose-related circulatory depression (decreased cardiac output and blood pressure)
o Dexmedetomidine modestly affects circulatory effects (decreased heart rate and systemic vascular resistance)

107
Q

Describe the circulatory effects of nitrous oxide and how it is affected by the use of other anesthetic agents

A

o Activates the sympathetic nervous system and increase SVR
o Activation of SNS leads to an increase in CVP and arterial pressure
o Sympathetic response appears to be intact during co-administration of volatile agents
o In contrast, when administered with opioids the addition of nitrous augments cardiac depression

108
Q

Describe the effect of moderate to high dose opioids on hemodynamics

A

Describe the effect of moderate to high dose opioids on hemodynamics

109
Q

Discuss possible mechanisms for hemodynamic effect of the opioids

A

o Most hemodynamic effects of opioids can be related to their influence on sympathetic outflow from the CNS

110
Q

Identify the opioid considered to have the most favorable effect on HR and BP for intubation and intraoperative BP control

A

o Sufentanil associated with lower heart rate and blood pressure during intubation

111
Q

Compare the effect of fentanyl and sufentanil on epinephrine and norepinephrine levels

A

o Norepinephrine
▪ Norepinephrine levels lower with sufentanil compared to other opioids
▪ Lower postoperative norepinephrine levels with sufentanil compared to other opioids, including fentanyl
o Epinephrine
▪ Lower intraoperative epinephrine levels with Demerol than with other opioids
▪ More consistent epinephrine levels with sufentanil, especially post-extubation

112
Q

List five effects of cardiopulmonary bypass on anesthesia drug disposition

A 
o Hemodilution
o Organ blood flow
o Protein binding
▪ Heparin
▪ Adjuvant drugs
o Sequestration in the lungs
113
Q

List three drugs classes commonly used as anti-ischemic therapy in patients with coronary artery disease (CAD)

A

o Nitrates
o Beta-Adrenergic Blockers
o Calcium Channel Blockers
o Effects of drugs complicated by stress of surgery, blood loss and anesthesia

114
Q

Describe the MOA of NTG in causing vasodilation

A

o Enter the smooth muscle and are converted to nitric oxide (NO)
o Smooth muscle relaxation results in vasodilation
o Enhances myocardial oxygen delivery and reduce demand
o NTG is primarily a venodilator

115
Q

List three beneficial effects of NTG in the patients with CAD

A

o Decrease wall tension
o Decrease myocardial O2 demand
o Decrease ischemia
 All improve cardiac function

116
Q

Discuss the dose dependent effects of NTG on the venous and arterial blood vessels

A

o More important effects of NTG are its systemic venous dilation
o Venous return is markedly reduced
 Decreased PCWP/LVEDP
 Improved compliance of LV
 Modifies position on Frank-Starling curve
o At larger doses, arterial vasodilation results

117
Q

Discuss how NTG may be better suited for pulmonary HTN than other more potent arterial vasodilators

A

o Vasodilation of pulmonary arteries and veins (more than systemic)
o Decreased RAP
o Decreased PAP
o Decreased PCWP
o Uses for pulmonary artery HTN (secondary or congenital PAH)

118
Q

Describe the unique effects of NTF on the coronary artery flow

A

o Potent coronary artery vasodilator
 Stenotic lesions vasodilate with NTG
 Smaller coronaries dilate more than larger
 Effectively reverse or prevents vasospasm

119
Q

Describe the use of NTG in improving coronary perfusion pressure (CPP)

A

o CBF may improve as PCWP decreases
 Reduces subendorcardial pressure
 CPP= DBP – PCWP
 Improved collateral flow

120
Q

Compare onset and duration for different administration routes of NTG

A
  1. SL NTG achieves blood levels within several minutes -> Last for 30-45 mins, bioavailability is 80%
  2. Oral NTG is unpredictable
  3. NTG ointment achieves blood levels within 20-30 minutes-> Last 4-6 hrs
  4. NTG patches -> slow onset up to 2 hours, levels maintained for 4 hours
  5. IV NTG -> instantaneous and may be titrate-> dose requirements vary between 50-150 mcg/minutes, higher doses may needed due to possible tolerance
121
Q

List five beneficial effects of beta blockade in patients with ischemic heart disease and their significance

A 
o	Reduction in myocardial oxygen consumption
o	Improved coronary blood flow
o	Prolonged diastole 
o	Improved collateral flow
o	Increased flow to ischemic area
o	?Membrane stabilization
o	Reduced mortality after MI
o	Improved oxygen dissociation 
o	? Inhibition of platelet aggregation
122
Q

Compare drugs with ISA to conventional beta blockers in regard to possible adverse consequences in patients with myocardial ischemia

A

o Anti-ischemic effects
o Anti-hypertensive effects
o Electrophysiologic effects -> ?membrane stabilization, increased VFIB threshold
o Metabolic effects
o Intrinsic Sympathomimetics Activity (ISA) -> elicits submaximal response, CO and HR are reduce less

123
Q

Discuss recommendations for perioperative beta blockade in patients with coronary disease

A

o Beta blockers should be continuous throughout perioperative period in patients with IHD
o Beta blockers should be titrated intraoperatively to heart rate and blood pressure in patients at risk for IHD
o Value of perioperative beta blockers is unknown for patients with risk factors for IHD even for vascular surgery

124
Q

List four potential adverse effects associated with perioperative beta blockade

A

o CHF -> potentiated by anesthetics, potentiated by other myocardial depressants such as CBD
o Bronchospasm
o ?Peripheral vasoconstriction
o ?Hypoglycemia
o Withdrawal associated with enhanced adrenergic activity -> tachycardia, HTN, myocardial ischemia

125
Q

List three mechanisms by which calcium blocking drugs (CBD’s) reduce myocardial oxygen demand

A

o Depression of contractility
o Decreased hr
o Decreased SBP (afterload)

126
Q

Compare diltiazem and verapamil to nicardipine and nifedipine in regard to clinical effects

A
  1. Nicardipine (Cardene) -> primary action on arterioles
     Does not decrease myocardial contractility
     Mild suppression of automaticity and conduction
     Selective for vascular smooth muscle, especially coronary and cerebral
     Dose 100-200 mcg bolus, 5-15 my/hr infusion
     Onset 2 minutes, half life 40 minutes
2.	Diltiazem 
	Coronary vasodilation 
	Some suppression of cardiac contractility 
	Suppression of SA node
	Suppression of AV node
3.	Verapamil 
	Coronary vasodilation
	Suppression of cardiac contractility 
	Suppression of SA node
	Suppression of AV node
127
Q

List three potential adverse effects associated with CBDs during during general anesthesia

A

o Hypotension
o Heart Failure
o Bradycardia
o Asystole
o AV block
o Potentiated by beta blockers, digitalis, volatile agents
o Withdrawal has been documented but rare

128
Q

List two mechanisms by which diuresis exert their anti-hypertensive effect

A

o Increase in urinary excretion of sodium
o Reduction in plasma volume and cardiac output
o After 6-8 weeks reduction in SVR due to activation of vascular endothelial potassium channels

o Inhibit sodium, chloride and potassium reabsorption, mild anti-HTN effect
o Use to treat CHF and excess intravascular fluid

129
Q

Discuss conventional thought on serum potassium and general anesthesia in patients on diuretics

A

o Most concerns relate to effects on fluid balance and electrolytes
o Rapid replacement of K+ is NOT recommended
 May produce life-threatening hyperkalemia
 Rapid replenishment is difficult (200-400 mEq to increase from 2.5 to 3.5)
 Chronic hypokalemia does NOT increase incidence of intraop dysrhythmias
o Serum K+ <3.O should NOT proceed with elective surgery

130
Q

Identify the first line anti-hypertensive for Heart Failure patients with HTN

A

o First line therapy for CHF, systemic HTN and mitral regurgitation is ACE inhibitors

131
Q

List four advantages of ACE inhibitors over conventional anti-hypertensives

A

o Free of CNS effects of antihypertensives
o Free of myocardial depression effects
o Metabolic changes are NOT seen
o Rebound HTN has NOT been seen

o May cause LVH to regress (inhibit remodeling)
o Hypotension has been observed upon induction

132
Q

List two hemodynamic concerns associated with ACEI and ARBs during general anesthesia

A

o ACEI and ARBs are increasingly replacing older meds are they are better tolerated
o Normal response to surgical stimulation may be attenuated (especially enalapril)
o Renin response to hemorrhage or hypotension will be impaired
o Angiotensin receptor blockers show similar issues
o Concomitant use of diuretic worsens the hypotension associated with ACEI or ARB

133
Q

Discuss alpha and beta receptor blockade associated with the use of Labetalol

A

o Blocks alpha-1, beta-1, beta-2
o Ratio 1: 6 alpha to beta
o Starting dose 2.5-5 mg IV

134
Q

Describe why thiosulfate is used with nitroprusside

A

o Sodium nitroprusside breaks done
 Release 5 cyanide ions
 Cyanide can prevent mitochondrial oxidative phosphorylat
o Rhodanase (enzyme) causes detoxification of cyanide
 Reacts with a sulfur donor
 Thiosulfate typically added to formulation
 Signs of toxicity include tachyphylaxis, metabolic acidosis

135
Q

List the typical dose of hydralazine

A

o Direct vasodilator-> Almost exclusively arterial vasodilation
o Typical dose 2.5-10 mg IV or IM

136
Q

List the onset time for hydralazine

A

o Slow onset (10 minutes after IV bolus) and offset (4 hours)

137
Q

Discuss three compensatory processes the body employs for HF

A
  1. Salt and water retention
     Augments preload via Frank-Starling Effect
     Causes pulmonary congestion and edema
  2. Vasoconstriction
     Maintains BP for perfusion of vital organs
     Exacerbates pump dysfunction by increasing afterload and MVOw
  3. Sympathetic stimulation
     Increases hr and blood ejection
     Increase dysrhythmias, MVO2
138
Q

List four classes of drugs used to treat HF that may interact with anesthesia agents

A 
o	Vasodilators
o	Diuretic 
o	Beta adrenergic receptor antagonists
o	Vasopressin-receptor antagonist
o	Dobutamine
o	PDE III
o	Digitalis 
o	Glucagon 
o	Triiodothyronine
139
Q

Identify the preferred beta blocker in patients with HF

A

o Carvedilol is preferred over metoprolol
o Convention is to administer beta blocker to all HF patients with EF < 40% who are stabilized on ACEI
o Starting dose should be small and if discontinued after prolonged administration should be tapered

o Activation of SNS contributes to the Pathophysiology of HF
o Wall stress, contractile dysfunction and remodeling predispose to dysrhythmias
o Ventricular function improves from better energetic and improved calcium utilization

CV Pharm (1 decks)

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