Pharm Ii, Exam 3

Front 1

What are the 4 steps in classifying asthma?

Back 1

step 1: mild intermittent asthma
step 2: mild persistent asthma
step 3: moderate persistent asthma
step 4: severe persistent asthma

Front 2

Step 1, Mild intermittent asthma

Back 2

- signs and symptoms <2x/wk, asymptomatic w normal peak flows between exacerbations, exacerbations brief w varying intensity, nighttime symptoms occur < 2x/mo., FEV1 or PEFR >80% of predicted value
- short-acting bronchodilator PRN, inhaled SABA are first line selection

Front 3

Step 2, Mild persistent asthma

Back 3

- s/s >2x/wk but <1x/day, exacerbations may affect activity, nighttime symtpoms occur > 2x/mo, FEV1 or PEFR </= 80% of predicted value
- long-term anti-inflammatory med, low dose inhaled corticosteroid; cromolyn or nedocromil particularly in chidlren; sustained-release theophylline as alternative; zafirlukast or zileuton for pts >12

Front 4

Step 3, Moderate persistent asthma

Back 4

- daily symptoms, daily use of SABA, exacerbations that affect activity occur >2x/wk and may last for days, nighttime symptoms occur > 1x/wk, FEV1 or PEFR 60-80% of predicted value
- long-term control meds; medium-dose inhaled corticosteroids or low to medium dose inhaled corticosteroids plus long-acting bronchodilator (inhaled or oral beta 2 agonist, sustained release theophylline), esp for nocturnal symptoms

Front 5

Step 4, severe persistent asthma

Back 5

- continuous s/s, frequent exacerbations, frequent nighttime symptoms, limited physical activity, FEV1 or PEFR < 60% of predicted value
- high-dose inhaled corticosteroids, long acting bronchodilators, systemic corticosteroids (prednisone)

Front 6

Who is the role of allergy in asthma greatest in?

Back 6

more in peds than adults

Front 7

What is the standard treatment found in steps 2, 3 and 4 of asthma?

Back 7

institute inhaled steroids

Front 8

How are most asthma drugs designed to be dosed?

Back 8

with 2 puffs

Front 9

Do you have to stress dose inhaled corticosteroids?

Back 9

not according to Johnny

Front 10

How long does it take for a SABA to kick in? (albuterol, levalbuterol, pirbuterol)

Back 10

incr airflow within 3-5 min

Front 11

Why is regularly scheduled daily use of SABA not recommended?

Back 11

the less you take, the better they work
more puffs leads to greater tolerance and down regulation of receptors -- will no longer be effective

Front 12

LABA (salmeterol, formoterol) should be used in combo with...

Back 12

inhaled corticosteroids
not recommended for monotherapy

Front 13

What are common causes of failure of asthma treatment?

Back 13

lack of adherence, comorbidities, ongoing exposure to tobacco smoke, airborne pollutants or allergens

Front 14

What is the preferred administration for LABAs?

Back 14

give in combo w inhaled corticosteroid mixed in same inhaler

Front 15

What are the best induction agents for asthma?

Back 15

if asthma w no active wheezing, use propofol
if actively wheezing and require EMERGENCY surgery, use ketamine bc it bronchodilates

Front 16

What things might you discover during the preop H and P that signal incr likelihood of intraop asthma difficulties?

Back 16

frequent nocturnal awakenings w dyspnea, recent incr in med dose/use, signs of viral infection

Front 17

What should you do if a non-emergent case presents w wheezing?

Back 17

postpone case until controlled

Front 18

What are the preop tests that can be done to assess current bronchoconstriction?

Back 18

FEV1 and PEFR

if values fall 30-50%, moderate bronchoconstriction
if <50% baseline, severe episode

Front 19

What pretreatment is advocated preop for asthmatics?

Back 19

systemic corticosteroid (prednisone or hydrocortisone)

Front 20

Complications associated with systemic corticosteroids given preop

Back 20

delayed wound healing, infection, adrenocortical insufficiency

Front 21

What are the most effective prophylactic drugs that can be given 20-30 min preop for asthmatics?

Back 21

anticholinergics - atropine and glycopyrrolate

mild bronchodilators

Front 22

What narcotic should be avoided in asthmatics?

Back 22

morphine- causes histamine release

fentanyl preferred!

Front 23

What GI meds should be avoided in asthmatics?

Back 23

H2 blockers - cimetidine/ranitidine/ famotidine
can cause bronchospasm due to loss of inhibitory feedback control via presynaptic H2 autoreceptor blockade -- incr histamine release

can give antihistamine if giving H1 (Benedryl) and H2 (reglan) together

Front 24

What's safer in asthmatics, regional or general?

Back 24

regional -- but! -- spinal or epidural level to midthoracic area or higher decr FRC, ERV, and ability to cough should be avoided

Front 25

How do IAs affect asthmatics?

Back 25

- IAs produce bronchial relaxation
- iso and des are resp irritants, blunt w opiates

Front 26

What NMB should be avoided in asthmatics?

Back 26

atracurium- histamine release
long-acting NMB can cause residual muscle weakness

Front 27

What cardiac meds should be avoided in asthmatics due to potential for bronchoconstriction?

Back 27

esmolol and labetalol

Front 28

What must be avoided in asthmatics with aspirin intolerance?

Back 28

toradol and other NSAIDs -- will cause asthma attack in these pts

Front 29

What should be done for an intraoperative bronchospasm?

Back 29

1. deepen level of anesthesia (IA, ketamine, propofol, lidocaine)
2. admin 100% Fi02
3. admin beta 2 agonist
4. epi IV or SC
5. IV corticosteroid
6. IV aminophylline if long-term postop mech vent planned

Front 30

What vent settings are preferred for general anesthesia in asthmatics?

Back 30

- avoid lung hyperinflation/barotrauma
- longer expiratory times
- decr Minute ventilation
- limited inspiratory time
- moderate permissive hypercapnia

Front 31

What is the emergence strategy for extubating an asthmatic?

Back 31

extubate at earliest possible time to prevent mechanical bronchial stimulation
give IV lidocaine and non-resp-depressing opiate dose to diminish airway sensitivity

Front 32

What is the most common time for intraop bronchoconstriction?

Back 32

emergence and extubation

Front 33

What are the major risk factors for incr intraop CV risk?

Back 33

- unstable coronary syndromes: acute (last 7 days) or recent (between last 7 and 30 days) MI; stable, unstable and severe angina
- decompensated heart failure: most formidable for anesthesia, class 4, worsening or new onset
- signficant arrhythmias: high-grade AV block, mobitz 2 block, 3rd deg AV Block, symtpomatic ventricular arrhythmias, SVT, AFib w RVR, symptomatic bradycardia, new vtach
- severe valvular disease: severe aortic stenosis, mean pressure gradient < 40 and valve are a< 1 cm^2 and symptomatic, mitral stenosis, progressive DOE, exertional syncope/HF

Front 34

What are the intermediate risk factors for incr intraop CV risk?

Back 34

- mild angina (Class 1,2)
- previous MI
- compensated/previous HF
- IDDM
- renal insufficiency

Front 35

What are the minor risk factors for incr intraop CV risk?

Back 35

- advanced age
- abnormal EKG (LV hypertrophy, LBBB, ST-T changes)
- Afib or other non-sinus rhythm
- low functional capacity (can't climb 1 flight of stairs)
- hx. CVA
- Uncontrolled HTN

Front 36

How effective are antiarrhythmics?

Back 36

only moderately successful, high side effect profile,
work by depressing the heart -- anesthetics also depress the heart

Front 37

How effective is ablation in treating arrhythmias?

Back 37

very successful

Front 38

Which drugs are antiarrhythmic vs arrhythmogenic?

Back 38

- drugs that depress heart, antiarrhythmic
- drugs that stimulate heart, positive ino/chrono/dromotropic, arrhythmogenic

Front 39

Class I antiarrhythmics

Back 39

- depressino of phase 0 depolarization, blocks Na channels like LAs

Front 40

Class II antiarrhythmics

Back 40

- beta blockers
- esmolol, propranolol, metoprolol, timolol, pindolol, atenolol, acebutelol, nadolol, carvidolol

Front 41

Class III antiarrhythmics

Back 41

- prolongs repolarization
- blocks K channels
- amiodarone, bretylium, sotalol, ibutilide, dofetilide

Front 42

Class IV antiarrhythmics

Back 42

- Ca channel blockers
- verapamil, diltiazem

Front 43

Adenosine works at _____ Receptors to cause a brief _______ in the SA and AV nodes, after which you hope to reestablish a regular rate.

Back 43

purine/purinergic,
cardiac arrest

Front 44

What antiarrhythmics are found in the "other" class?

Back 44

- adenosine (for SVT), ATP, digoxin (For afib), atropine

Front 45

The greater the prolongation of depolarization and repolarization, the more _____ the drug.

Back 45

antiarrhythmic

Front 46

Torsaades is associated with marked ...?

Back 46

prolonged QT?

Front 47

How are symptomatic bradyarrhythmias treated?

Back 47

pacers

Front 48

What is the first line treatment for ectopic beats and tachycardia?

Back 48

beta blockers

Front 49

What are the treatment goals for afib?

Back 49

- anticoagulation (blood pools and tends to form clots -- if pt converted out of afib without anticoag, they will throw emboli)
- ventricular rate control
- maintain sinus rhythm w meds (amiodarone)
- RF ablation (complications of CVA, cardiac tamponade, esophageal injury)

Front 50

How are ventricular tachycardias treated?

Back 50

vtach: IV drugs if hemodynamically stable, or cardioversion
vfib: defibrillation

Front 51

What is the preffered drug for ventricular dysrhythmia?

Back 51

amiodarone, lidocaine

Front 52

What is the preferred treatment for heart block?

Back 52

atropine, pacing

Front 53

What is the preferred treatment for atrial tachyarrhythmia (afib/flutter)?

Back 53

verapamil (beta blocker or dig)

Front 54

What is the preferred treatment for torsaades de pointes?

Back 54

magnesium

Front 55

What is the preferred treatment for sinus tachycardia?

Back 55

esmolol

Front 56

Why should you start with lower doses of antiarrhythmic drugs in the OR?

Back 56

anesthetics are already myocardial depressing

Front 57

Which drug should be avoided for treating intraop SVT?

Back 57

adenosine

Front 58

What is the recommended treatment for VT or VF in a pt w structural heart dz?

Back 58

implantable cardioverter/defibrillator (ICD)

Front 59

When does chronic HTN create the greatest perioperative issue?

Back 59

when emerging and recovering the patient -- in pain, shivering, bucking while trying to extubate can all incr HR and BP

Front 60

Clonidine, moxonidine, and methyldopa all inhibit _____.

Back 60

baroreceptor discharge

Front 61

What do diuretics promote?

Back 61

Na excretion, decrease volume

Front 62

What are the 3 mechanisms of action of beta blockers?

Back 62

central depression in medulla, cardiac depression, renin inhibition

Front 63

Spironolactone is a ______ inhibitor.

Back 63

aldosterone

Front 64

Losartan (ARB), alpha blockers, Ca channel blockers, nitric oxide, and endothelin-1 all work to ...

Back 64

decrease peripheral vascular resistance

Front 65

Normal BP classification

Back 65

SBP <120, DBP <80
no antiHTN drugs indicated

Front 66

Prehypertensive classification

Back 66

120-139/80-89
encourage lifestyle mod.
no antiHTN drugs indicated

Front 67

Stage 1 HTN classification

Back 67

140-159/90-99
lifestyle mod.
thiazide diuretics, may add ACEI, ARB, BB, CCB

Front 68

Stage 2 HTN classification

Back 68

>160/>100
lifestyle mod.
2 drug combo with thiazide diuretic and ACEI/ARB/BB/CCB
subclassified into urgent (>180 and fix within 24 hrs) and emergent (fix ASAP)

Front 69

Why are pts often noncompliant with anti-HTN drugs?

Back 69

large side effect profile, frequent dosing

Front 70

ACE inhibitors prevent the conversion of ____ to ____.

Back 70

AT 1 to AT 2

Front 71

What active compound is the most potent vasoconstrictor?

Back 71

AT 2 - works on AT 1 receptors

Front 72

What are the 4 main classes of anti-HTN drugs?

Back 72

1. diuretics
2. ACE inhibitor (reduce Na load and produce vasodilation)
3. ARBs (direct antagonist, vasodilation)
4. Ca channel blockers (central and cardiac depr, vasodilation)
(BB were recently dropped off the list)

Front 73

____ is a good treatment for intraop HTN, but if they're asthmatic, _____ is a good alternative.

Back 73

labetalol, hydralazine

Front 74

What are some non-pharmacologic measures that can be employed to manage HTN?

Back 74

keep pts warm, prevent shivering
elevate HOB
encourage void if no foley
pain mgmt to prevent fluctuating BP

Front 75

What is the drug of choice if the patient is HTN and tachycardic?

Back 75

labetalol (decr HR)

Front 76

What is the drug of choice if the pt is HTN with a HR 60s?

Back 76

hydralazine (incr HR)

Front 77

What are the primary differences between esmolol and labetalol?
What is metoprolol good for?

Back 77

- labetalol alpha and beta blocker (vasodilates), esmolol only beta blocker (Vasoconstricts)
- labetalol lasts longer (3-6 hrs) than esmolol (<20 min)
- esmolol metabolized in plasma by RBC esterase
-Metoprolol is good for asthmatic (cardioselective)

Front 78

_____ is an alternative to beta blockers that causes direct arterial dilation. It takes 10-30 min for onset, so do not re-dose until you've waited at least this long!

Back 78

hydralazine

Front 79

What is the most important consideration in caring for someone receiving chronic beta blockade?

Back 79

- make sure no doses are missed preop/intraop/postop
- pts on b-blockers up-regulate, if abruptly stopped --> develop major rebound HTN, angina, tachycardia
- must be tapered, never abruptly D/C'ed

Front 80

Where is nipride metabolized?

Back 80

by Hgb in the plasma

Front 81

What is the metabolite of nipride? How is it eliminated?

Back 81

free cyanide in bloodstream --> detox in body when combined w thiosulfate in liver by the rhodanese enzyme --> converts CN to thiocyanate to be excreted in urine

Front 82

What happens if a pt gets excess nipride?

Back 82

can't metabolize their CN fast enough, develop histotoxic hypoxia (Tissues cant utilize O2 in cells) --> give methylene blue, Na nitrate, and Na thiosulfate

Front 83

How does cyanide cause histotoxic hypoxia?

Back 83

blocks cytochrome oxidase

Front 84

Na nitroprusside is a direct ______ or both ___ and ____, causing release of ____ to cause rapid onset decr in BP.

Back 84

-vasodilator
-arteries and veins
-nitric oxide

Front 85

What two classes of anti-HTN meds cannot be given in pregos?

Back 85

ACE inhibitors and ARBs -- can cause fetal death!

Front 86

What is the cause of rebound HTN following cessation of nipride?

Back 86

renin release

Front 87

What are the s/s of cyanide toxicity?

Back 87

CNS dysfunction (mental status change, seizure, coma)
CV instability (tachyphylaxis, HTN, arrythmias)
incr metabolic acidosis, incr lactate

Front 88

How is suspected cyanide toxicity treated?

Back 88

1. stop infusion of SNP
2. 100% FiO2
3. mech ventilation PRN
4. NaHCO3 to correct acidosis
5. Na nitrite, Na thiosulfate, methylene blue

Front 89

ARBs are given to patients who cannot tolerate ____.

Back 89

ace inhibitors

Front 90

What is the first line therapy for HTN pts? What is its limitation?

Back 90

thiazide diuretics (cheap, convenient),
pts develop tolerance after approx 1 wk, initially causes diuresis which decr blood volume

Front 91

_____ Are less effective in black people, but help preserve renal function in pts w diabetic or non-diabetic nephropathy

Back 91

Ace inhibitors

(acei, arbs, and b-blockers all less effective in blacks)

Front 92

What active compound is the most potent vasoconstrictor?

Back 92

AT 2 - works on AT 1 receptors

Front 93

What are the 5 mechanisms for lowering BP?

Back 93

1. central depr
2. cardiac depr
3. baroreceptor depr
4. hormonal depr
5. vasodilation

IAs have all 5 of these mechanisms!

Front 94

Ace inhibitors end in ____ and ARBs end in ____.

Back 94

-pril
-sartan

Front 95

Pts may not be able to tolerate ACE inhibitors because of this side effect: ______. They should then be given ____, which do not affect bradykinin to cause this side effect, although more expensive.

Back 95

cough, ARBs

Front 96

2 main vasodilators are ____ which helps with afterload, and ____ which helps with preload.

Back 96

hydralazine afterload,
NTG preload

Front 97

Nebivolol, contains ___ to aid in vasodilation.

Back 97

nitric oxide

Front 98

Ca channel blocker MOA

Back 98

*central and direct acting with vasodilation*
vasodilation and decr peripheral resistance, central depression, negative chrono/ino/dromotropic,
decr Ca so decr contractility,

tx for HTN and arrythmias

Front 99

What is the MOA for cental alpha agonist clonidine?

Back 99

decr catecholamine release as a presynaptic alpha 2 agonist
watch out for rebound HTN w missed dose

Front 100

A good non-cardiac drug for treating preop anxiety in HTN pts is

Back 100

versed

Front 101

Angina is caused by

Back 101

a mismatch between supply and demand of coronary blood flow

Front 102

_____ is the most common cardiac disease, is progressive, and drug therapy becomes less effective with time.

Back 102

CAD

Front 103

What are the 2 possible MOAs of anti-anginal drugs?

Back 103

1. vasodilate to incr coronary blood supply
2. decr cardiac demand and depress the heart (more effective)

Front 104

Nitrates for angina

Back 104

first-line therapy for acute attacks, decr O2 demand with reduction in preload and beneficial redistribution of blood flow

Front 105

Beta blockers for angina

Back 105

cornerstone therapy for chronic prophylaxis, decr cardiac demand by lowering HR, BP and contractility

Front 106

Ca Channel blockers for angina

Back 106

esp effective in variant angina and pts tolerant to B-blockers
reduce preload/afterload and incr coronary flow

Front 107

Antiplatelet drugs for angina

Back 107

asa inhibits platelet and endothelial COX,
reduces coronary thrombosis,
plavix may be substituted in pts w contraindication to asa

Front 108

Statins for angina

Back 108

HMG-CoA reductase inhibitor,
reduce c-reactive protein, thrombogenicity, and adverse cardiac effects

Front 109

ACE inhibitors for angina

Back 109

useful in pts w CAD and DM or other vascular diseases

Front 110

Ranolazine for angina

Back 110

given in conjunction with standard antianginals, blocks late inward Na current reducing intracellular Ca overload

Front 111

What are the 4 classes of angina pectoris?

Back 111

1. mild, angina does not occur w ordinary physical activity, but may occur w strenuous, rapid or prolonged exertion
2. slight limitation of ordinary activity
3. marked limitation of ordinary physical activity, comfortable at rest
4. severe, inability to carry out any physical activity without discomfort, angina may be present at rest

Front 112

What conditions decrease myocardial O2 supply?

Back 112

1. decr coronary blood flow (tachycardia at expense of diastole, hypotension, hypocapnia w coronary vasoconstriction, coronary artery spasm)
2. decr O2 content and availability (anemia, hypoxemia, Left o2 shift)

Front 113

What conditions incr O2 demand?

Back 113

-***tachycardia***
- incr wall tension (incr preload/afterload)
- incr myocardial contractility

most drugs address this rather than decr O2 supply

Front 114

If heart ischemia lasts < ___ min, the heart muscle should reperfuse and recover. If longer, MI develops.

Back 114

15 minutes

Front 115

____ are shown to reverse plaque buildup and open vessels, causing regression in CAD, pts should remain on these drugs intraop. and preop.

Back 115

statins

Front 116

What kind of angina am i?
predictable chest pain with HR > 125
fixed lesion
pt learns how much physical exertion needed to elicit symptoms

Back 116

stable

Front 117

Which angina am i?
have both plaques and spasms
exercise induced, occurs also at rest, night pain, EKG changes

Back 117

unstable

Front 118

Which angina am i?
vasospasms alone, occurs at rest, occurs in clusters during early AM, ST elevation, rarely exercise induced

Back 118

variant (spasmotic)

Front 119

What is the primary prevention for angina?

Back 119

control: high chol, DM, HTN, smoking
give: asa, statins

Front 120

What is the treatment for stable angina?

Back 120

improve O2 demand/supply mismatch
BB, CBB, nitrates, antiplatelet agents, statins, ACEI, revascularization w PCI/CABG

Front 121

What is the treatment for UA/NSTEMI?

Back 121

asa/clopidogrel
BB, CCB, Heparin, nitrates, GP2B3A inhibitors, revascularization w PCI/CABG

Front 122

What is the treatment for STEMI?

Back 122

fibrinolytics, asa/clopidogrel, heparin, nitrates, GP 2A3B inhibitors, revascularization with PCI/CABG

Front 123

What is the treatment for secondary prevention and long term care after plaque rupture from UA/NSTEMI/STEMI?

Back 123

- asa/clopidogrel
- BB, ACEI, statins
- ICD w EF < 35%
- revascularization w PCI/CABG

Front 124

What is the MOA of nitrates?

Back 124

*decr preload/afterload by vasodilation*
*increase supply, reduce demand*
dilate epicardial coronary stenosis
decr Coronary artery resistance
blocks spasm
incr collateral flow to ischemic areas
primarily dilates veins to decr venous blood returning to heart and decr preload, decr myocardial O2 demand

Front 125

What is the best way to decrease preload after giving nitrates?

Back 125

sit pt up in a chair and keep legs lower than heart

Front 126

The #1 drug to maintain CAD and prevent long-term attacks is ______, with a goal HR of ____.

Back 126

b-blockers, 50-60

Front 127

What are the effects of cardioselective beta 1 blockade?

Back 127

bradycardia, renin suppression, reduced free fatty acids, bronchodilation, vasodilation, glycogenolysis

Front 128

What drug should be avoided in variant angina, because it may worsen vasospasms with vasoconstriction?

Back 128

nonselective beta blockers

Front 129

What are the treatment guidelines for prophylactic preop beta blockers?

Back 129

- start 1 wk before sx if possible (bisoprolol, metoprolol, atenolol) 1month best
- titrate to target HR 55-70
- use half dose if HR < 65, SBP < 120, elderly or frail
- hold if HR <55 or SBP <100
- continue b-blocker 1-4 wks postop and taper to d/c
- before incr dose, consider other sources of tachycardia (pain, bleeding, sepsis)

Front 130

What pt population is most benefitted by preop b-blocker prophylaxis?

Back 130

high risk pts having vascular surgery

Front 131

Which vasodilating drugs work only on arteries, veins, or both?

Back 131

arterial- hydralazine
venous- NTG (Releases NO)
both- all other vasodilating agents affect both arterial and venous vascular beds

Front 132

What is the MOA for Ca channel blockers in treating myocardial ischemia?

Back 132

blocking Ca entry in to Ca channels will decr contractility, and decr O2 demand
decr smooth muscle tone to cause vasodilation and incr O2 supply
*increase supply, decrease demand*
*vasospastic angina*

Front 133

What are the drugs of choice or variant and stable angina?

Back 133

variant- Ca channel blockers
stable- beta blockers

Front 134

What is the MOA for nitrates?

Back 134

release of NO to vasodilate

Front 135

No matter what revascularization technique is used, ____ is the lifelong therapy staple.

Back 135

aspirin

Front 136

What herbal meds affect coag and hemostasis?

Back 136

3 g's!
garlic, ginkgo biloba, ginseng

inhibit plt aggregation and have anticoag effects
ask pts to stop taking garlic 1 wk preop, 48 hrs preop stop ginkgo and ginseng

Front 137

The primary antianginal drug for prior infarct or heart failure is..

Back 137

beta blockers

Front 138

What is the highest morbidity disorder that someone can have undergoing surgery?

Back 138

CHF

Front 139

What are the components of triple therapy in CHF pts?

Back 139

ACEI, b-blocker, diuretics (aldosterone antagonist or loop)

Front 140

What are the 4 classes of CHF?

Back 140

1. mild, no limitation, ordinary physical exercise does not cause fatigue, dyspnea or palpitations
2. slight limitation of physical activity, comfortable at rest but ordinary activity results in fatigue, palpitations or dyspnea
3. marked limitation of physical activity, comfortable at rest but less than ordinary activity results in symptoms
4. severe, unable to carry out any physical activity without discomfort, symptoms persist at rest, incr discomfort w any level of activity -- need a heart transplant!

Front 141

_____ should be used in all CHF pts, as it can improve symptoms, decr hospitalization and MI, and prolong survival. If not tolerated because of coughing side effect, the alternative is _____

Back 141

ACEI, ARB

Front 142

______ can decrease the symptoms of heart failure, improve exercise tolerance, and decr hospitalization, but does NOT improve survival.

Back 142

digoxin (glycoside)

Front 143

What combo of drugs can be added in black patients taking ACEI and b-blockers for class 3-4 CHF?

Back 143

hydralazine and isosorbide (vasodilators)

Front 144

What are the 5 inotropic mechanisms that can be manipulated for CHF?

Back 144

1. beta 1 agonism (dopamine, dobutamine)
2. Na/K ATPase inhibition (Digoxin, incr ca influx and contractility)
3. incr Ca
4. PDE-3 inhibition (milrinone)
5. glucagon

Front 145

What is the MOA of PDE inhibitors for CHF pts?

Back 145

increases cAMP and increases Ca, to incr contractility

Front 146

Digoxin inhibits the _____ pump to encourage ___ To move intracellularly and improve myocardial contraction.

Back 146

Na-K ATPase, Ca

Front 147

What is a normal digoxin level?

Back 147

0.5-2.0, with goal of 1.2-1.5 depending on renal fcn

start w low doses to follow closely and monitor for arryhthmias

Front 148

What are the side effects associated with digoxin?

Back 148

- arrhythmias of all sorts
- confusion, restless, colored vision
- NVD, anorexia

Front 149

Digoxin has a ____ inotropic and ______ chronotropic effect, causing the heart to beat harder and slower. Its onset is ____, making it less useful in anesthesia, designed more for chronic use

Back 149

positive ino, neg chrono, slow onset (24hrs)

Front 150

Digoxin has a long half life of ___, taking ____ Days until it is excreted.

Back 150

36-48 hrs, 5-7 days

Front 151

What does it mean that digoxin has a therapeutic index of 1?

Back 151

same dose that is therapeutic in 1 pt is toxic in another pt
LD50=ED50
difficult to give therapeutically and titrate without toxicity

Front 152

How does K level influence digoxin toxicity?

Back 152

- incr K level means less digoxin will bind to Na-K ATPase (less likely to show toxicity)
- decr K level means more drug binds to receptor Na pump (more likely to show toxicity)

K level is inversely proportional to digoxin, receptor binding regardless of dig level

Front 153

What are the digoxin considerations for anesthesia?

Back 153

- why taking the drug? (for atrial tachyarrhythmia or CHF inotropy?)
- dig level
- serum K (if < 3.0 give K IV minibag)
- efficacy (how is it working?)

very long acting, so less crucial if missed preop, but better if taken

Front 154

If you have to do an emergency induction on a CHF pt, the best method is...

Back 154

slow induction with reduced doses, use dopamine/dobutamine, vasodilators and diuretics, treat symptoms as they arise

Front 155

What are the two types of medications that should generally be held preop?

Back 155

- anti-diabetic medications
- anticoagulants if possible

Front 156

What can be given IV for life-threatening dig toxicity?

Back 156

digibind within 30-60 min

give w overdose >10 mg in adults, > 4 mg in children levels
give w hyperK in dig toxic pt
give for life-threatening arrhythmias (vtach, vfib, severe brady or heart bolck unresponsive to atropine or pacing)

Front 157

Elective surgery should be postponed for at least __ weeks for bare-metal stent
-Elective surgery should be postponed for at least __ year for drug-eluting stent

Back 157

-6 weeks
-1 year

Front 158

antiplatelet therapy should be maintained in all situations in which the risk of bleeding is low. The exceptions are?

Back 158

-intracranial surgery
-posterior eye surgery
-massive bleeding

Front 159

Patients whose symptoms are mild and infrequent can use a _____ for relief of asthma symptoms.

Back 159

short acting beta angonist (SABA)
-also for acute exacerbation

Front 160

Patients with more frequent cough, wheezes, chest tightness, SOB should use a?

Back 160

-inhaled coricosteroid (long term controller med)
-prophylaxis

Front 161

For asthma patients who remain symptomatic despite compliance with inhaled corticosteroids, the addition of a _____ is recommended,. Higher doses may be needed.

Back 161

long acting beta agonist or leukotriene modifiers

Front 162

_____ are used for rapid relief of asthma symptoms or for prevention of exercise induced.

Back 162

SABA

Front 163

In all age groups with persistent asthma, _____ are the most effective long term treatment.

Back 163

inhaled corticosteroids
-prevention-

Front 164

ARBS are antihypertensive because?

Back 164

-they block angiotensin receptors--> angiotensin can't bind-->can't increase BP

Front 165

The main side effect of ACE inhibitors is bradykinin can't be broken down this leads to a sometimes severe ____.

Back 165

cough
-in pts who develop cough, switch to ARBs

Front 166

Common side effects of BB are?

Back 166

-cold extremities due to vasoconstriction (avoid in PVD)
-lower blood sugar (avoid in diabetes)
-bronchoconstriction (avoid in asthma)

Front 167

What are the common blood tests to obtain in chronic stable ischemic heart disease (angina)

Back 167

-lipid levels
-metabolic eval (glucose and creatinine, thyroxine, HbA1C)
-Markers of cardiac inflammation (CRP, BNP)
-Prothrombic assessment

Front 168

B1 receptors cause what things to happen?

Back 168

-cardiac stimulation
-renin release
-lipolysis

Front 169

B2 receptors cause what things to happen?

Back 169

-bronchodilation
-vasodilation
-glycogenolysis

Front 170

When a nonselective Beta blocker is given (blocking 1 and 2) what happens?

Back 170

-bradycardia
-renin supression
-reduced free fatty acids
-bronchospasm
-vasoconstriction
-reduced energy

Front 171

when a Beta 1 selective beta blocker is given, what happens?

Back 171

-bradycardia
-renin suppression
-reduced free fatty acids
-bronchodilation
-vasodilation
-glycogenolysis

Front 172

Intrinsic sympathomimetic activity (ISA) causes what to happen?

Back 172

-less resting bradycardia
-less bronchospasm?
-less HDL reduction
-Less Post-MI benefit?

Front 173

In anesthesia avoiding ____ is necessary.

Back 173

tachycardia
-keep them vasodilated, pain meds, hydrated.

Front 174

Beta blockers treat angina by?

Back 174

causing cardiac depression and decreasing the HR, heart doesn't work as hard.