• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/301

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

301 Cards in this Set

  • Front
  • Back
What are the 4 steps in classifying asthma?
step 1: mild intermittent asthma
step 2: mild persistent asthma
step 3: moderate persistent asthma
step 4: severe persistent asthma
Step 1, Mild intermittent asthma
- 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
Step 2, Mild persistent asthma
- 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
Step 3, Moderate persistent asthma
- 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
Step 4, severe persistent asthma
- 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)
What does it indicate if SABA is used > 2x/wk for symptomatric relief?
indicates inadequate control and need to step up treatment
When diagnosing or changing between each step of asthma, what must be done with the patient?
pt education, assess adherence, environmental control, management of comorbidities
For steps 2-4 of asthma, what should be considered for administration for pts with allergic asthma?
subcutaneous allergen immunotherapy
When assessing the management of an asthmatic, you can step down if possible after asthma has been well controlled for how long?
3 months
Why is zileuton a less desirable alternative?
because of limited studies as adjunctive therapy and the need to monitor liver fcn.
When prescribing theophylline, what must be monitored?
serum concentration levels
What environmental allergens are responsible for allergic asthma?
house dust mites, animal danders, pollens
possibly molds and cockroaches
Evidence is strongest for immunotherapy with...
single allergens
Who is the role of allergy in asthma greatest in?
more in peds than adults
Clinicians who admin immunotherapy or omalizumab should be prepared and equipped for what complication?
identification and treatment of anaphylaxis
What are the adverse effects associated with systemic corticosteroid therapy for asthma?
acne
adrenal suppression and insufficiency
avascular necrosis of the femoral head
behavioral disturbances
cushingoid habitus (moon face, buffalo hump, central obesity)
ecchymosis
fluid/lyte imbalance
growth suppression in kids
hirsutism (hairy)
hyperglycemia
HTN
incr susceptibility to infection
myopathy
osteoporosis
Peptic ulcers
posterior subcapsular cataracts
striae
What is the standard treatment found in steps 2, 3 and 4 of asthma?
institute inhaled steroids
How are most asthma drugs designed to be dosed?
with 2 puffs
What is the treatment for acute bronchoconstriction?
inhaled short acting beta 2 agonist
What is the treatment for chronic bronchoconstriction?
inhaled steroids, most beneficial in lowest effective doses (more effective than SABA, leukotriene modifiers, LABA, cromolyn or theophylline in improving pulmonary function, preventing symptoms and exacerbations, reducing need for ED treatment, and decr deaths due to asthma)
What are the adverse effects noted with inhaled corticosteroids?
oral thrush, respiratory irritation, dysphonia, hoarseness, reflex cough, bronchospasm

w high doses- monitor for osteoporosis and cataracts
Do any clinically significant changes occur i the hypothalamic pituitary adrenal axis function with low or medium dose steroids?
no, but childrens growth should be monitored
Do you have to stress dose inhaled corticosteroids?
not according to Johnny
How long does it take for a SABA to kick in? (albuterol, levalbuterol, pirbuterol)
incr airflow within 3-5 min
Why is regularly scheduled daily use of SABA not recommended?
the less you take, the better they work
more puffs leads to greater tolerance and down regulation of receptors -- will no longer be effective
What are the adverse effects associated with SABAs?
systemic toxicity (high dose or elderly), paradoxical bronchospasm, tachycardia, skeletal muscle tremor, headache, hypoK, hyperglycemia
LABA (salmeterol, formoterol) should be used in combo with...
inhaled corticosteroids
not recommended for monotherapy
Can you use a LABA to relieve acute allergy symptoms?
no
What adverse effects are associated with LABAs?
cause down-regulation of beta 2 receptor w loss of the bronchoprotective effect from rescue therapy with a SABA

high doses produce tremor, tachycardia, QT prolongation, hypoK, hyperglycemia
Leukotriene modifiers can be used as an alternative to ______ for persistent asthma but they are _____.
inhaled corticosteroids, less effective
Can leukotriene modifiers (motelukast, zafirlukast) be used for an acute asthma exacerbation?
no - dose response curve is flat
What are the adverse effects associated with leukotriene modifiers?
churg-strauss vasculitis (more from corticosteroid withdrawal though)
suicidal ideation, hepatitis/liver failure, can incr coumadin and theophylline levels w coadministration
What lab value must be monitored w leukotriene modifiers?
liver enzymes, particularly ALT
When is cromolyn sodium used?
mild persistent asthma, not popular, less effective than inhaled corticosteroids but safer side effect profile
When and how is theophylline administered?
for persistent asthma, alone or with inhaled corticosteroid
What is the desired serum theophylline level?
5-15 mcg/mL
What is the drawback of theophylline?
interactions w a lot of drugs, causing either incr metabolism and decr effectiveness OR decr metabolism and incr toxicity
What are the side effects associated with theophylline?
common: N/V, nervous, headache, insomnia
serious: hypoK, hyperglycemia, tachycardia, arrhythmia, tremor, NM irritability, seizures, death
Why are anticholinergics (Ipratropium bromide, spiriva) used in asthmatics?
inhaled short acting bronchodilator for COPD (alternative if pt cant tolerate SABA)
What are the side effects associated with inhaled anticholinergics?
dry mouth, pharyngeal irritation, urinary retention, incr IOP
In what pts should anticholinergics be avoided?
glaucoma, BPH, bladder neck obstruction
Omalizumab subcutaneous injection
recombinant humanized monoclonal antibody that prevents IgE from binding to mast cells and basophils, preventing release of inflammatory mediators after allergen exposure

pt must be at least 12, specific allergies, moderate to severe persistent asthma

fewer exacerbations, expensive
Why does omalizumab have a black box warning?
anaphylaxis -- must monitor pt 2 hours after first 3 injections, then 30 min after subsequent injections
What is the preferred treatment for pregnant asthmatics?
Albuterol SABA- excellent safety profile
inhaled corticosteroids for long term control
What are common causes of failure of asthma treatment?
lack of adherence, comorbidities, ongoing exposure to tobacco smoke, airborne pollutants or allergens
What is the preferred administration for LABAs?
give in combo w inhaled corticosteroid mixed in same inhaler
What are the best induction agents for asthma?
if asthma w no active wheezing, use propofol
if actively wheezing and require EMERGENCY surgery, use ketamine bc it bronchodilates
What things might you discover during the preop H and P that signal incr likelihood of intraop asthma difficulties?
frequent nocturnal awakenings w dyspnea, recent incr in med dose/use, signs of viral infection
What should you do if a non-emergent case presents w wheezing?
postpone case until controlled
What are the preop tests that can be done to assess current bronchoconstriction?
FEV1 and PEFR

if values fall 30-50%, moderate bronchoconstriction
if <50% baseline, severe episode
What pretreatment is advocated preop for asthmatics?
systemic corticosteroid (prednisone or hydrocortisone)
Complications associated with systemic corticosteroids given preop
delayed wound healing, infection, adrenocortical insufficiency
What are the most effective prophylactic drugs that can be given 20-30 min preop for asthmatics?
anticholinergics - atropine and glycopyrrolate

mild bronchodilators
What narcotic should be avoided in asthmatics?
morphine- causes histamine release

fentanyl preferred!
What GI meds should be avoided in asthmatics?
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
What's safer in asthmatics, regional or general?
regional -- but! -- spinal or epidural level to midthoracic area or higher decr FRC, ERV, and ability to cough should be avoided
How do IAs affect asthmatics?
- IAs produce bronchial relaxation
- iso and des are resp irritants, blunt w opiates
What NMB should be avoided in asthmatics?
atracurium- histamine release
long-acting NMB can cause residual muscle weakness
What cardiac meds should be avoided in asthmatics due to potential for bronchoconstriction?
esmolol and labetalol
What must be avoided in asthmatics with aspirin intolerance?
toradol and other NSAIDs -- will cause asthma attack in these pts
What should be done for an intraoperative bronchospasm?
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
What vent settings are preferred for general anesthesia in asthmatics?
- avoid lung hyperinflation/barotrauma
- longer expiratory times
- decr Minute ventilation
- limited inspiratory time
- moderate permissive hypercapnia
What is the emergence strategy for extubating an asthmatic?
extubate at earliest possible time to prevent mechanical bronchial stimulation
give IV lidocaine and non-resp-depressing opiate dose to diminish airway sensitivity
What is the most common time for intraop bronchoconstriction?
emergence and extubation
Should you reverse NMBs with an anticholinesterase in asthmatics?
not if can be avoided w using short-acting paralytics -- if must give anticholinesterase must also give atropine/glycopyrrolate to ensure total blockade of parasympathomimetic side effects
How should a pregnant asthmatic be treated intraop?
avoid parenteral beta agonists, maintain maternal oxygenation, avoid non-emergency surgery until delivery (until after first trimester if semi-emergent)
use antacids but not H2 blockers
minimize hypotension (uterine displacement, generous fluid replacement, compression stockings, leg elevation)
if must vasopressor, use ephedrine
avoid N20
shield fetus from radiography
use fetal monitoring and U/S when possible
Preop, asthmatics should be encouraged to stop smoking for at least ____ prior to surgery.
8 wks
What should you do if a respiratory infection is present in an asthmatic preop?
admin abx and delay surgery
In asthmatics, surgery should be minimzed to ____ hrs if possible.
3 hrs
_____ surgical technique is preferred w asthmatics.
laparoscopic
What are the post op considerations for asthmatics?
encourage IS/deep breathing
use continuous positive airwya pressure
use intercostal nerve blocks and LA infiltration of incisional area for pain PRN
What are the signs of atropine poisoning?
red as a beet, blind as a bat, dry as a bone, mad as a hatter, hot as a hare
Which anticholinergic causes sedation?
atropine
Which anticholinergic is better for drying secretions?
glycopyrrolate, esp w ketamine
Which anticholinergic increases HR more?
atropine
Which anticholinergic relaxes smooth muscle and decr GI H+ ion secretion more?
both equally
Which anticholinergic causes mydriasis/cycloplegia?
atropine
Which anticholinergic is best for preventing motion induced nausea?
atropine (Scopalamine best!)
What is the primary difference between atropine and glycopyrrolate?
atropine crosses BBB and placenta

glycopyrrolate is not lipid soluble, 100% ionizied -- no PO absorption, cannot pass BBB/placenta, better in pregnancy
Effects of beta 1 agonists
-headache, dizzy, nervous
- sweating
- incr HR, incr force of ctx, cardiac disturbances (pos. ino/chrono/dromotropic)
- constipation
- incr BP, incr lipid level from lipolysis
Effects of beta 2 agonists
- restless, headache
- bronchodilation (albuterol)
- tachycardia
- tremor
- relaxation of pregnant uterus
- incr blood flow to heart muscle, brain, skeletal muscle (vasodilation)
- incr blood glucose levels and insulin secretion
Effects of alpha 1 agonists (phenylephrine)
- ocular decongestion, nasal decongestion, goosebumps, constipation
- restless, headache, sweating, pupil dilation, nervous
- reflex bradycardia, cardiac dysrhythmia, vasoconstriction, incr BP
- urinary retention
How do beta 1 agonists incr BP?
renin release incr BP
What are the effects of alpha antagonists (phentolamine, regitine)?
- headache, drowsy, nasal congestion, pupil constriction
- reflex tachy, vasodilation, decr BP
- incr peristalsis, promotes micturition, impotence

reserved for old guys w HTN and BPH, shrinks prostate
postural hypotension
What are the effects of beta antagonists?
- lassitude, nightmares, deprssion, loss of libido
- bronchoconstriction
- negative ino/chrono/dromotropic, decr BP
- decr blood glucose
- incr peristalsis and flatulence
Both alpha 1 and beta 2 antagonists induce ____ Synthesis.
glycogen -- decr glucose levels
Effects of muscarinic antagonists/anticholinergics (atropine, glycopyrrolate)?
- decr cognition, sedation, facial flushing, pupil dilation, incr IOP, dry mouth
- incr HR, bronchodilation, inhibition of mucous secretions
- decr peristalsis and secretions, decr gastric juice secr., urinary retention
What are the major risk factors for incr intraop CV risk?
- 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
What are the intermediate risk factors for incr intraop CV risk?
- mild angina (Class 1,2)
- previous MI
- compensated/previous HF
- IDDM
- renal insufficiency
What are the minor risk factors for incr intraop CV risk?
- 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
What perioperative medical therapy can be done to decr CV risk?
- beta blockers: esp in vascular surgery
- statins
- alpha 2 adrenergic blockers
- nitro and dilt not effective
What preoperative coronary revascularization techniques can be done to decr CV risk?
- percutaneous revascularizaiton w angioplasty (may incr complications)
- CABG: mod effectiveness in select pts
What perioperative monitoring techniques can be done to decr CV risk?
- PA cath: only during open cardiac sx, incr complications
- CVP, 12-lead, and TEE not seen as effective
What anesthetic techniques can be employed to decr CV risk factors?
- epidural anesthesia and analgesia
- intraop normothermia
High risk non cardiac surgical procedures (>5%)
- aortic/major vascular surgery
- peripheral vascular surgery
Intermediate risk noncardiac surgeries (1-5%)
carotid endarterectomy
head and neck surgery
intraperitoneal/intrathoracic surgery
ortho sx
prostate sx
Low risk noncardiac surgeries (<1%) -- do not require further preop cardiac testing
endoscopy, superficial procedures, cataract sx, breast sx, ambulatory sx
The SA and AV nodes are controlled by _____.
calcium
Atrial muscle and ventricular cells depolarize due to _____.
sodium
Ventricular arrhythmias are generated by an abberation w ____.
sodium (use class 1 or 3 antiarrhythmic)
What is the MOA of verapamil?
slows AV conduction, will cause a heart block, which is desirable in AFib
Beta1 blockade the heart is (positive/negative) chrono/ino/dromotropic?
negative to all!
What is the approach to treating arrhythmias that develop intraop?
get them out of the OR safely, treat when symptomatic VS fluctuations
How effective are antiarrhythmics?
only moderately successful, high side effect profile,
work by depressing the heart -- anesthetics also depress the heart
How effective is ablation in treating arrhythmias?
very successful
Which drugs are antiarrhythmic vs arrhythmogenic?
- drugs that depress heart, antiarrhythmic
- drugs that stimulate heart, positive ino/chrono/dromotropic, arrhythmogenic
What structural heart diseases may cause intraop rhythm disturbance?
- CAD
- MI
- valvular and congenital heart dz
- cardiomyopathy
- Sick sinus or long QT syndrome
- WPW syndrome
- heart dz secondary to systemic dz (uremia, DM)
- sinus brady
- AV block
What transient imbalances may cause intraop rhythm disturbance?
- stress: electrolyte or metabolic imbalance
- laryngoscopy, hypoxia, hypercarbia
- device malfcn/microshock (bovie, pacer)
- diagnostic or therapeutic interventions (pacer, cardioverter/defib)
- surgical stim
- central venous cath (Can tickle atria)
Class I antiarrhythmics
- depressino of phase 0 depolarization, blocks Na channels like LAs
Class IA antiarrhythmics
- moderate depression and prolongs repol.
- quinidine, procainamide, disopyramide
Class IB antiarrhythmics
- weak depression and shortens repolarization
- lidocaine, mexiletine, phenytoin, tocainide
Class IC antiarrhythmics
- strong depression w little effect on repol
- flecainide, propafenone, moricizine
Class II antiarrhythmics
- beta blockers
- esmolol, propranolol, metoprolol, timolol, pindolol, atenolol, acebutelol, nadolol, carvidolol
Class III antiarrhythmics
- prolongs repolarization
- blocks K channels
- amiodarone, bretylium, sotalol, ibutilide, dofetilide
Class IV antiarrhythmics
- Ca channel blockers
- verapamil, diltiazem
Adenosine works at _____ Receptors to cause a brief _______ in the SA and AV nodes, after which you hope to reestablish a regular rate.
purine/purinergic,
cardiac arrest
What antiarrhythmics are found in the "other" class?
- adenosine (for SVT), ATP, digoxin (For afib), atropine
The greater the prolongation of depolarization and repolarization, the more _____ the drug.
antiarrhythmic
What effects are produced by adenosine acting on purine receptors to inhibit adenyl cyclase?
- slowing of SA and AV conduction
- bronchoconstriction
- dilation of cerebral and coronary vessels
- modulation of NT release
Adenosine works at _____ Receptors to cause a brief _______ in the SA and AV nodes, after which you hope to reestablish a regular rate.
purine/purinergic,
cardiac arrest
What antiarrhythmics are found in the "other" class?
- adenosine (for SVT), ATP, digoxin (For afib), atropine
The greater the prolongation of depolarization and repolarization, the more _____ the drug.
antiarrhythmic
What effects are produced by adenosine acting on purine receptors to inhibit adenyl cyclase?
- slowing of SA and AV conduction
- bronchoconstriction
- dilation of cerebral and coronary vessels
- modulation of NT release
Torsaades is associated with marked ...
prolonged QT
How are symptomatic bradyarrhythmias treated?
pacers
What is the first line treatment for ectopic beats and tachycardia?
beta blockers
What causes regular narrow complex tachycardia? how is it treated?
AV nodal reentry due to accessory pathway

adenosine, verapamil, diltiazem, beta blockers, RF cath ablation
What are the treatment goals for afib?
- 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)
How are ventricular tachycardias treated?
vtach: IV drugs if hemodynamically stable, or cardioversion
vfib: defibrillation
What is the preffered drug for ventricular dysrhythmia?
amiodarone, lidocaine
What is the preferred treatment for heart block?
atropine, pacing
What is the preferred treatment for atrial tachyarrhythmia (afib/flutter)?
verapamil
What is the preferred treatment for torsaades de pointes?
magnesium
What is the preferred treatment for sinus tachycardia?
esmolol
Why should you start with lower doses of antiarrhythmic drugs in the OR?
anesthetics are already myocardial depressing
Which drug should be avoided for treating intraop SVT?
adenosine
What is the recommended treatment for VT or VF in a pt w structural heart dz?
implantable cardioverter/defibrillator (ICD)
What is the preferred treatment for preventing a pt from going into AFib and maintaining sinus rhythm, vs the preferred treatment for rate control to prevent an Afib pt from going into RVR?
prevention of Afib - amiodarone
prevention of converting to Afib w RVR and rate control- verapamil
_____ inhibits CYP3A4, causing prolonged activity or toxicity in several other drugs, cardiac and otherwise.
amiodarone
______ help control the ventricular rate in Afib/flutter, and terminate and prevent recurrences of paroxysmal SVT.
beta blockers
____ is an IV cardioselective beta blocker, administered as a _____, commonly given post cardiac surgery.
esmolol, infusion -- hypotension and bradycardia resolve within 30 min of D/Cing infusion
When are Ca channel blockers contraindicated?
WPW syndrome
What is the major sign of toxicity when giving sotalol, dofetilide, and ibutilide?
torsaades de pointes
Flecainide and propafenone markedly decrease _____.
cardiac conduction velocity
Digoxin cannot be used in patients with _____.
wpw syndrome
When does chronic HTN create the greatest perioperative issue?
when emerging and recovering the patient -- in pain, shivering, bucking while trying to extubate can all incr HR and BP
Clonidine, moxonidine, and methyldopa all inhibit _____.
baroreceptor discharge
What do diuretics promote?
Na excretion
What are the 3 mechanisms of action of beta blockers?
central depression in medulla, cardiac depression, renin inhibition
Spironolactone is a ______ inhibitor.
aldosterone
Losartan (ARB), alpha blockers, Ca channel blockers, nitric oxide, and endothelin-1 all work to ...
decrease peripheral vascular resistance
Normal BP classification
SBP <120, DBP <80
no antiHTN drugs indicated
Prehypertensive classification
120-139/80-89
encourage lifestyle mod.
no antiHTN drugs indicated
Stage 1 HTN classification
140-159/90-99
lifestyle mod.
thiazide diuretics, may add ACEI, ARB, BB, CCB
Stage 2 HTN classification
>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)
Why are pts often noncompliant with anti-HTN drugs?
large side effect profile, frequent dosing
HTN is silent until it causes _____.
end organ damage
HTN is a symptom of whatever disease is causing it, such as...
CNS control in medulla, kidney disease, heart dz, vascular dz, baroreceptor problems
What are the major CV risk factors?
HTN,
smoking
obesity (BMI > 30)
physical inactivity
dyslipidemia
DM
microalbuminuria, GFR < 60
age > 55 men, >65 women
fam hx of premature CV dz
What are the sites for target organ damage in HTN?
1. heart: LV hypertrophy, angina, prior MI, prior coronary revascularization, HF
2. brain: CVA or TIA
3. chronic kidney dz
4. peripheral arterial dz
5. retinopathy
What are the most identifiable causes of HTN?
OSA
drug-induced
chronic kidney disease
primary aldosteronism
renovascular dz
chronic steroid therapy, cushings syndrome
pheochromocytoma
aortic coarctation
thyroid/parathyroid dz
What are the lifestyle modifications indicated for HTN management, in order of effectiveness?
smoking cessation, weight reduction, DASH diet, Na restriction, exercise, moderate etoh consumption
What are the causes for resistant HTN?
improper BP measurement
volume overload and pseudotolerance
drug-induced
non-adherence #1
associated conditions (obesity, excessive ETOH)
What is the drug of choice for HTN in pregnancy?
central alpha agonist (methyldopa)

hydralazine if given IV
can use beta blockers (atenolol, metoprolol, labetalol)
diuretics only if chronic
ACE inhibitors prevent the conversion of ____ to ____.
AT 1 to AT 2
What active compound is the most potent vasoconstrictor?
AT 2 - works on AT 1 receptors
What are the 5 main classes of anti-HTN drugs?
1. diuretics
2. B blockers (central and cardiac depr, renin inhibitor)
3. ACE inhibitor (reduce Na load and produce vasodilation)
4. ARBs (direct antagonist, vasodilation)
5. Ca channel blockers (central and cardiac depr, vasodilation)
____ is a good treatment for intraop HTN, but if they're asthmatic, _____ is a good alternative.
labetalol, hydralazine
What are some non-pharmacologic measures that can be employed to manage HTN?
keep pts warm, prevent shivering
elevate HOB
encourage void if no foley
pain mgmt to prevent fluctuating BP
What is the drug of choice if the patient is HTN and tachycardic?
labetalol (decr HR)
What is the drug of choice if the pt is HTN with a HR 60s?
hydralazine (incr HR)
What are the primary differences between esmolol and labetalol?
- 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
What is the drug of choice for pheochromocytoma?
phentolamine
_____ 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!
hydralazine
What is the most important consideration in caring for someone receiving chronic beta blockade?
- 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
IV drug choices available for HTN emergencies:
Na nitroprusside, nicardipine, clevidipine, fenoldopam, labetalol, NTG, esmolol, phentolamine, hydralazine
Where is nipride metabolized?
by Hgb in the plasma
What is the metabolite of nipride? How is it eliminated?
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
What happens if a pt gets excess nipride?
can't metabolize their CN fast enough, develop histotoxic hypoxia (Tissues cant utilize O2 in cells) --> give methylene blue, Na nitrate, and Na thiosulfate
How does cyanide cause histotoxic hypoxia?
blocks cytochrome oxidase
Na nitroprusside is a direct ______, causing release of ____ to cause rapid onset decr in BP.
vasodilator, nitric oxide
What two classes of anti-HTN meds cannot be given in pregos?
ACE inhibitors and ARBs -- can cause fetal death!
What is the cause of rebound HTN following cessation of nipride?
renin release
What are the s/s of cyanide toxicity?
CNS dysfunction (mental status change, seizure, coma)
CV instability (tachyphylaxis, HTN, arrythmias)
incr metabolic acidosis, incr lactate
How is suspected cyanide toxicity treated?
1. stop infusion of SNP
2. 100% FiO2
3. mech ventilation PRN
4. NaHCO3 to correct acidosis
5. Na nitrite, Na thiosulfate, methylene blue
ARBs are given to patients who cannot tolerate ____.
ace inhibitors
What is the first line therapy for HTN pts? What is its limitation?
thiazide diuretics (cheap, convenient),
pts develop tolerance after approx 1 wk, initially causes diuresis which decr blood volume
____ are more effective than thiazide diuretics in pts with moderate to severe renal insufficiency.
loop diuretics
Potassium-sparing diuretics such as amiloride are particularly useful for...
pts w hypoK
Spironolactone is a ____ sparing diuretic that antagonizes _____.
K-sparing, aldosterone
_____ Are less effective in black people, but help preserve renal function in pts w diabetic or non-diabetic nephropathy
Ace inhibitors

(acei, arbs, and b-blockers all less effective in blacks)
What is the drug of choice for HTN in pregnancy?
central alpha agonist (methyldopa)

hydralazine if given IV
can use beta blockers (atenolol, metoprolol, labetalol)
diuretics only if chronic
ACE inhibitors prevent the conversion of ____ to ____.
AT 1 to AT 2
What active compound is the most potent vasoconstrictor?
AT 2 - works on AT 1 receptors
What are the 5 main classes of anti-HTN drugs?
1. diuretics
2. B blockers (central and cardiac depr, renin inhibitor)
3. ACE inhibitor (reduce Na load and produce vasodilation)
4. ARBs (direct antagonist, vasodilation)
5. Ca channel blockers (central and cardiac depr, vasodilation)
____ is a good treatment for intraop HTN, but if they're asthmatic, _____ is a good alternative.
labetalol, hydralazine
What are the 5 mechanisms for lowering BP?
1. central depr
2. cardiac depr
3. baroreceptor depr
4. hormonal depr
5. vasodilation

IAs have all 5 of these mechanisms!
In pregnancy, these two meds cause pressor resistant hypotension during induction, and are teratogenic?
acei and arb
Ace inhibitors end in ____ and ARBs end in ____.
-pril
-sartan
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.
cough, ARBs
What does it mean if a drug is cardio-selective beta blocker?
blocks beta 1 in heart, not beta 2 in rest of body -- no vasoconstriction, bronchoconstriction or hypoglycemia
What is ISA activity?
intrinsic sympathomimetic activity seen in beta blockers -- partial agonists, lower efficacy and not as potent, but also have decr side effects; better with diabetic and asthmatic pts
What are the 3 main side effects of beta blockade?
1. precaution w asthmatics due to bronchoconstriction
2. vasoconstriction - incr afterload and exacerbates vascular disease/claudication
3. causes hypoglycemia - blocks SNS production of sugar in liver (Caution in diabetics)
What is the MOA of beta blockers?
central depr in medulla, cardiac depr on beta receptors in heart, block renin release in kidneys
Labetalol has the 3 typical MOAs of beta blockers, plus...
direct vasodilation
In low dose beta blockers (bisoprolol, atenolol, metoprolol...), you can achieve ______, which lessens with increased dosing.
cardioselectivity for beta 1 in heart
2 main vasodilators are ____ which helps with afterload, and ____ which helps with preload.
hydralazine afterload,
NTG preload
What is the benefit of using beta blockers with alpha blocking properties?
prevents as much vasoconstriction, alpha blockers vasodilate, causing less work on the heart, less claudication, and better BP control
ex: labetalol, carvedilol
Nebivolol, contains ___ to aid in vasodilation.
nitric oxide
Ca channel blocker MOA
vasodilation and decr peripheral resistance, central depression, negative chrono/ino/dromotropic,
decr Ca so decr contractility,

tx for HTN and arrythmias
Alpha blockers such as prazosin, terazosin, and doxazosin are reserved for what population?
HTN and enlarged prostate -- watch out for postural/ortho. hypotension
Why is reserpine avoided for treatment of HTN?
causes depression
What is the MOA for cental alpha agonist clonidine?
decr catecholamine release as a presynaptic alpha 2 agonist
watch out for rebound HTN w missed dose
A good non-cardiac drug for treating preop anxiety in HTN pts is
versed
What are some intraop techniques for reducing BP?
incr IA, incr Propofol, low dose labetalol
Angina is caused by
a mismatch between supply and demand of coronary blood flow
_____ is the most common cardiac disease, is progressive, and drug therapy becomes less effective with time.
CAD
What are the 2 possible MOAs of anti-anginal drugs?
1. vasodilate to incr coronary blood supply
2. decr cardiac demand and depress the heart (more effective)
Nitrates for angina
first-line therapy for acute attacks, decr O2 demand with reduction in preload and beneficial redistribution of blood flow
Beta blockers for angina
cornerstone therapy for chronic prophylaxis, decr cardiac demand by lowering HR, BP and contractility
Ca Channel blockers for angina
esp effective in variant angina and pts tolerant to B-blockers
reduce preload/afterload and incr coronary flow
Antiplatelet drugs for angina
asa inhibits platelet and endothelial COX,
reduces coronary thrombosis,
plavix may be substituted in pts w contraindication to asa
Statins for angina
HMG-CoA reductase inhibitor,
reduce c-reactive protein, thrombogenicity, and adverse cardiac effects
ACE inhibitors for angina
useful in pts w CAD and DM or other vascular diseases
Ranolazine for angina
given in conjunction with standard antianginals, blocks late inward Na current reducing intracellular Ca overload
What are the 4 classes of angina pectoris?
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
What conditions decrease myocardial O2 supply?
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)
What is the HTN treatment of choice in black people?
Ca channel blockers with diuretics combo.
What conditions incr O2 demand?
- tachycardia
- incr wall tension (incr preload/afterload)
- incr myocardial contractility

most drugs address this rather than decr O2 supply
If heart ischemia lasts < ___ min, the heart muscle should reperfuse and recover. If longer, MI develops.
15 minutes
What are the ischemic cascade symptoms?
effort --> ischemia --> diastolic dysfunction --> systolic dysfunction --> EKG changes and dyspnea --> pain --> take NTG for pain relief --> EKG normalizes --> systolic recovery starts --> stunning --> full recovery
What are the symptoms, duration, and response to activity in angina?
symptoms: pressure/tightness/ heaviness; diffuse pain; burning sensation; substernal/precordial; radiates to arms, shoulder, elbow, wrist, jaw, back, abdomen
duration: 1-15 min -- if longer, MI with plaque rupture
response to activity: precipitated by exertion, relieved promptly by rest
____ are shown to reverse plaque buildup and open vessels, causing regression in CAD, pts should remain on these drugs intraop. and preop.
statins
What kind of angina am i?
predictable chest pain with HR > 125
fixed lesion
pt learns how much physical exertion needed to elicit symptoms
stable
Which angina am i?
have both plaques and spasms
exercise induced, occurs also at rest, night pain, EKG changes
unstable
Which angina am i?
vasospasms alone, occurs at rest, occurs in clusters during early AM, ST elevation, rarely exercise induced
variant
If pt has angina, a good diagnostic tool is to ask
when they get chest pain
What EKG change is associated with stable angina?
ST depression
What is the primary prevention for angina?
control: high chol, DM, HTN, smoking
give: asa, statins
What is the treatment for stable angina?
improve O2 demand/supply mismatch
BB, CBB, nitrates, antiplatelet agents, statins, ACEI, revascularization w PCI/CABG
What is the treatment for UA/NSTEMI?
asa/clopidogrel
BB, CCB, Heparin, nitrates, GP2B3A inhibitors, revascularization w PCI/CABG
What is the treatment for STEMI?
fibrinolytics, asa/clopidogrel, heparin, nitrates, GP 2A3B inhibitors, revascularization with PCI/CABG
What is the treatment for secondary prevention and long term care after plaque rupture from UA/NSTEMI/STEMI?
- asa/clopidogrel
- BB, ACEI, statins
- ICD w EF < 35%
- revascularization w PCI/CABG
What is the MOA of nitrates?
decr preload/afterload
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
What is the best way to decrease preload after giving nitrates?
sit pt up in a chair and keep legs lower than heart
What are the side effects of NTG?
- causes headaches
- produces rapid tolerance and stops being efficient -- only use as a rescue agent
- dizzy, palpitations, hypotension
What is the contraindication for nitrates?
significant/symptomatic hypotension
The #1 drug to maintain CAD and prevent long-term attacks is ______, with a goal HR of ____.
b-blockers, 50-60
What are the effects of cardioselective beta 1 blockade?
bradycardia, renin suppression, reduced free fatty acids, bronchodilation, vasodilation, glycogenolysis
What drug should be avoided in variant angina, because it may worsen vasospasms with vasoconstriction?
nonselective beta blockers
By using a beta blocker with ISA, you cause less....
less resting bradycardia
less bronchospasm
less HDL reduction
less post-MI benefit
What occurs in beta blockers that have membrane stabilizing activity (MSA)? - propranolol and acebutolol
good antiarrhythmic
antiplatelet effects
What are the treatment guidelines for prophylactic preop beta blockers?
- start 1 wk before sx if possible (bisoprolol, metoprolol, atenolol)
- 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)
What pt population is most benefitted by preop b-blocker prophylaxis?
high risk pts having vascular surgery
Which vasodilating drugs work only on arteries, veins, or both?
arterial- hydralazine
venous- NTG (Releases NO)
both- all other vasodilating agents affect both arterial and venous vascular beds
What is the MOA for Ca channel blockers in treating myocardial ischemia?
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
What are the drugs of choice or variant and stable angina?
variant- Ca channel blockers
stable- beta blockers
What is the MOA for nitrates?
release of NO to vasodilate
What side effects are most closely associated with statins?
muscle pain, myoglobin production, may damage liver (lipitor more popular among MDs than zocor for lower side effect profile)
What are the 2 types of stents?
drug eluting stents (DES)
bare metal stents (BMS)
How do platelets lead to pathological atherosclerosis?
platelets normally flow through vessels without sticking to walls (prevented by endothelium and prostacyclin)
after vascular injury, exposes VWF and collagen, which activates platelets and they adhere to vessel walls --> degranulate and release mediators (TXA2 and ADP) to form a platelet rich thrombus to prevent blood loss at site of vessel injury
What is the most common cocktail to treat pathologic atherosclerosis?
asa (inhibits cox 1) and
plavix (inhibits ADP receptor to inhibit plt function)
synergistic combo
What are the 3 classes of anti-platelet drugs?
- asa (Blocks COX, analgesic, antiplatelet)
- ADP receptor antagonist (plavix)
- Glycoprotein 2b3a inhibitor (Given for angioplasty and stenting IV at time of procedure, reopro and integralin, prevents plt aggregation)
What are the intraop risk factors for thrombosis w DES?
- stents in L main coronary artery
- stents in bifurcations
- greater total stent length
- heightened plt activity (Surgery, malignancies, DM)
- in-stent restenosis
- LV dysfunction
- localized hypersensitivity vasculitis
- penetration of stent into necrotic core
- renal dz
- DM
- resistance to anti-plt meds
- inappropriate d/c of anti-plt therapy
What are the preop considerations for pts with coronary artery stents?
- type, when placed, where located, if complicated procedure
- hx of stent thrombosis
- antiplatelet regimen
- comorbidities
- consult w interventional cardiologist
What is the duration of antiplt therapy for dilation without stenting?
2-4 wks dual antiplt, postpone sx 2-4 wks if possible
What is the duration of antiplt therapy for PCI and BMS?
4-6 wks dual antiplt, postpone sx 6-12 wks and operate before restenosis could occur
What is the duration of antiplt therapy for PCI and DES?
12 mo dual-antiplt therapy and surgery postponed 12 mo.
No matter what revascularization technique is used, ____ is the lifelong therapy staple.
aspirin
What are the 2 components of dual antiplatelet therapy?
thienopyridine and asa

in emergency surgery, continue asa and hold thienopyridine, but restart the latter asap
Clopidogrel is indicated in all patients after ____ or those with ____ intolerance/resistance.
PCI, asa
What are the anesthetic mgmt techniques for angina/ischemia?
- ischemia is masked by anesthesia (Ekg changes are a late sign)
- avoid tachycardia (Esp induction and emergence) - exacerbates ischemia
- avg person w CAD will not exhibit ischemia w HR <120, goal HR 55-70
- maintain BP/HR as close to preop baseline as possible
- esmolol helpful during induction and emergence to manage VS
- keep pt warm, relaxed and pain free w HOB elevated during emergence/postop
- if see ST changes, give NTG
What herbal meds affect coag and hemostasis?
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
What are the regional anesthesia considerations in the anticoagulated pt?
- stop taking asa 48 hrs prior to block
- d/c plavix 1 wk prior to block (pt might throw a clot in the meantime!)
- d/c GP2B3A inhibitors 8-48 hrs prior to block
- can start IV heparin 1 hr after needle placement
- with epidurals, remove 2-4 hrs after last heparin dose and verify PTT/INR prior to cath d/c
The primary antianginal drug for prior infarct or heart failure is..
beta blockers
What are the components of triple therapy in pts with angina of effort?
short-acting nitrates, beta blocker, ca channel blocker (monitor for Hypotension)
When is CABG indicated?
failure to respond to medical therapy
L mainstem lesion
triple vessel dz
reduced LV fcn
Failure to respond to nitrates in angina of effort patients may be due to...
nitrate tolerance, worsening dz, poor compliance
What is the highest morbidity disorder that someone can have undergoing surgery?
CHF
What are the components of triple therapy in CHF pts?
ACEI, b-blocker, diuretics (aldosterone antagonist or loop)
What are the 4 classes of CHF?
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!
What are the signs of poor LV function?
- CHF w wet lungs and dyspnea
- recent or multiple infarctions
- cardiac index < 2L/min/m^2
- LVEDP > 15 mmHg
- ventricular dysrhythmias
- areas of hypokinesis/akinesis
- dyskinesia or aneurysm in ventriculogram or echo
What are the 5 factors affecting CO?
1. rate (most important, incr HR at expense of diastolic filling, decr CO)
2. rhythm (decr filling and function)
3. preload (frank starling - incr ventricular filling will incr contractility to a point of overdistension, after which O2 demand increases and contractility is impaired)
4. afterload (reduced by incr wall thickness from compensatory hypertrophy)
5. ventricular contractility (inotropic state)
_____ 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 _____
ACEI, ARB
Cardiac remodeling
heart changes structure to improve function (compensatory)
______ can decrease the symptoms of heart failure, improve exercise tolerance, and decr hospitalization, but does NOT improve survival.
digoxin (glycoside)
What combo of drugs can be added in black patients taking ACEI and b-blockers for class 3-4 CHF?
hydralazine and isosorbide (vasodilators)
What are the 5 inotropic mechanisms that can be manipulated for CHF?
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
What is the MOA of PDE inhibitors for CHF pts?
increases cAMP and increases Ca, to incr contractility
Digoxin inhibits the _____ pump to encourage ___ To move intracellularly and improve myocardial contraction.
Na-K ATPase, Ca
What is a normal digoxin level?
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
What are the side effects associated with digoxin?
- arrhythmias of all sorts
- confusion, restless, colored vision
- NVD, anorexia
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
positive ino, neg chrono, slow onset (24hrs)
Digoxin has a long half life of ___, taking ____ Days until it is excreted.
36-48 hrs, 5-7 days
What does it mean that digoxin has a therapeutic index of 1?
same dose that is therapeutic in 1 pt is toxic in another pt
LD50=ED50
difficult to give therapeutically and titrate without toxicity
How does K level influence digoxin toxicity?
- 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
What are the digoxin considerations for anesthesia?
- 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
What are the classes of drugs indicated for intraop CHF mgmt?
- RAAS antangonists (acei, arb)
- nitrovasodilators
- direct vasodilators
- ca channel blocker
- PDE inhibitor (milrinone)
- sympathomimetic (dopamine, dobutamine)
- sympatholytic (labetalol)
If you have to do an emergency induction on a CHF pt, the best method is...
slow induction with reduced doses, use dopamine/dobutamine, vasodilators and diuretics, treat symptoms as they arise
What are the two types of medications that should generally be held preop?
- anti-diabetic medications
- anticoagulants if possible
What can be given IV for life-threatening dig toxicity?
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)