Exam 3 Flashcards
Antidysrhythmics, beta blockers, calcium channel blockers, itraconazole
negative inotropes and may worsen HF
cyclophosphamide (Cytoxin), daunorubicin (cerubidine), doxorubicin (adriamycin)
cardiotoxic and may worsen HF
androgens, estrogens, glucocorticoids, NSAIDS, rosiglitazone (Avandia), pioglitazone (Actos)
drugs that cause increased blood volume and may worsen HF
6 mechanisms of action against HF
adrenergic blockers cardiac glycosides phophodiesterase inhibitors vasodilators ACEI and ARBs Diuretics
adrenergic blockers
treat HF by decreasing cardiac workload by slowing HR (B1) and decreasing BP (A1)
Carvedilol
Cardiac Glycosides
treat HF by increasing cardiac output by increasing the force of myocardial contraction
Digoxin
Phophodiesterase inhibitors
treat HF by increasing CO by increasing force of myocardial contraction
Milrinone
Carvedilol
adrenergic blocker-treats HF
Digoxin
cardiac glycoside treats HF
milrinone
phophodiesterase inhibitor treats HF
vasodilators
treat HF by decreasing cardiac workload by dilating vessels and reducing preload
isosorbide dinitrate with hydralazine
ACEI and ARBs
treat HF by increasing CO by lowering BP and decreasing blood volume
lisinopril
Diurectics
treat HF by increasing CO by reducing fluid volume and decreasing blood pressure
furosemide
isosorbide dinitrate with hydralazine
vasodilator to treat HF by decreasing cardiac workload by dilating vessels and reducing preload
lisinopril
ACEI or ARB that treats HF by increasing CO by lowering BP and decreasing blood volume
furosemide
diuretic that treats HF by decreasing fluid volume and BP to increase CO
nitrates aspirin clot-preventing drugs beta blockers statins Calcium channel blockers
drugs to manage angina pectoris
Nitroglycerin
dilates veins and arteries
decrease myocardial workload
decrease preload (pooling of blood in periphery)
decrease myocardial ischemia to prevent vasospasm and dilates coronary arteries to increase perfusion
can be used for prevention of treatment
action of nitroglycerin
inactivate myosin and permissive vasodilation or relaxation of vessel tone occurs
Nitrates side effects/teaching
orthostatic hypotension
headaches, dizziness, vertigo, flushing, sweating
with the onset of angina, sit down and place on NTG tab under the tonge and wait 3-5 mins. If the angina has not subsided, take another tablet sublingually and wait 3-5 mins. If the angina has not subsided, take a third tablet and call 911 for help. Notify physician immediately.
Metoprolol, labetalol, propanolol
beta blockers for treatment of stable angina prevention
IV or PO
decrease HR, BP, contractility
cardioprotective
afterload of heart is reduced due to vasodilation
perfusion is improved through the coronaries bc of vasodilation and prolonged diastole
the heart can experience a greater Ejection Fraction due to prolonged diastolic filling time
Calcium Channel Blockers
diltiazem (Cardizem)
verapamil (Calan, Isoptin)
nifedipine (procardia, Adalat)
PO
Action of CCBs
decrease SA node automaticity and AV conduction to decrease HR and myocardial contractility
Decrease HR, BP, cause vasodilation, decrease preload and afterload, decrease myocardial oxygen needs
side effects of CCbs
Cardiovascular-hypotension, palpitations, and tachycardia
GI-constipation and nausea
Other-rash, flushing, and peripheral edema
Ranolazine (Ranexa)
can be used alone or with other angina meds, such as CCBs, beta blockers, or nitroglycerin
Unlike some other angine meds, Ranexa can be used with oral erectile dysfunction meds
Ranexa changes the metabolism of myocardium from fatty acid use for fuel to glucose, thereby decreasing metabolic needs
Treatment of Stable Angina
NTG, Beta Blockers, CCBs, ACEIs
treatment of unstable angina
NTG, heparin, clopidogrel, morphine, ASA
treatment of Prinzmetals angina
NTG and CCbs
Goals for treatment of MI (5)
reperfusion of blood supply to damage myocardium
reduce myocardial oxygen demand
control and prevent future myocardium dysrythmias
reduce post MI mortality
manage pain
10 drug classes to manage MI
thrombolytic agents aspirin ADP receptor blockers Glycoprotein IIb/IIIa Inhibitors anticoagulants nitrates beta blockers ACEIs and ARBs Pain management (morphine or demerol) statins-post MI
OANM
oxygen aspirin nitroglycerin morphine treatment of MI
Thrombolytics
directly break up clots; give within 30 mins-12 hours following MI enhance activation of plasminogen streptokinase (Streptase) alteplase (tPA, Activase) anistrplase (Eminase) reteplase (Retevase) tenecteplase (TNKase)
thrombolytics contraindications
active bleeding or known bleeding d/o Hx of hemorrhagic stroke or intracranial vessel malformation recent major surgery or trauma uncontrolled HTN Pregnancy
enoxaparin (Lovenox)
LMWH
fibrinolysis should be started within 12 hrs to treat MI
Post MI care
ACEI/ARB
ASA or Antiplatelet agent
beta blocker or CCB
Statin
Captopril (Capoten)
Enalapril (Vasotec)
Benazepril (Lotensin)
Fosinpril (Monopril)
ACEI
Aspirin
Clopidogrel (Plavix)
Ticlopidine (Ticlid)-rarely used, neutropenia
antiplatelet agents
Prevent cardiac remodeling
beta blockers Metoprolol (Lopressor) Atenolol (Tenormin) Propranolol Esmolol Labetalol
Amlodipine (Norvasc)
Diltiazem (Cardizem, Adalat)
CCBs
Statins action
lower cholesterol lovastatin (Mevacor) pravastatin (Pravachol) simvastatin (Zocor) atorvastatin (Lipitor)
Dihydropyridine
treats MI?
nifdeipine (Adalat, Procardia XL)
blocks Calcium channels in the vascular smooth muscle decreasing the amount of intracellular calcium available for muscle contraction this results in the fall of BP
decrease myocardial oxygen demand due to the reduced afterload
Nondihydropyridines
verapamil (Calan, Isoptin)
Block l type calcium channels in vascular smooth muscle causing vasodilation
verapamil and diltiazem block calcium channels in the myocardium decreasing the rate of conduction reducing the HR reducing the contractility of the myocardium
benefit of Ranolazine (Ranexa)
effect on HR is minimal as the drug acts on myocardial metabolism
Nitrates adverse effects
secondary to vasodilation: headache, flushing, orthostatic hypotension
potential cardiovascular collapse if mixed with alcohol
nitrates disadvantage
tolerance builds quickly
What happens if you D/C a long acting nitroglycerin (Isosorbide dinitrate) abruptly?
vasospasm
nitrates contraindications
preexisting hypotension, head trauma (vasodilation would make these worse)
pericardial tamponade and constrictive pericarditis (vasodilation would make heart unable to maintain CO to maintain BP)
no sustained release tabs on pts with glaucoma (nitroglycerin may increase introcular pressure)
caution severe kidney/liver disease (toxic levels)
dehydration and hypovolemia should be corrected before nitroglycerin is administered (severe hypotension may occur)
Nitrate drug interactions
viagra none within 24 hrs before or after-cardiovascular collapse–>hypotension
ethanol, CCBs, antidepressants, phenothiazines, and anti HTN may cause additive Hypotension
sympathomimetics (EPI) antagonize vasodilation
Do you take beta blockers for Prinzmetals angina
no, they make it worse
Beta Blockers action in treating Angina
prevention
decrease HR, BP, contractility, workload
cardioprotective
Why beta blockers over nitrates for prevention of angina?
tolerance not an issue
possess antidysrythmic properties
ideal for common disorder combo of HTN and CAD
cardioprotective
when to DC beta blockers
gradually unless fatigue, lethargy, and depression occur
With long term care, the heart becomes more sensitive to catecholamines, which are blocked by beta blockers. when w/d abruptly, adrenergic receptors are activated and rebound excitation occurs. In pts with CAD, this can exacerbate angina, precipitate tachycardia, or cause an MI
beta blockers adverse effects at high doses?
SOB and respiratory distress secondary to bronchoconstriction therefore use caution with asthma and COPD pts
Beta blockers and diabetes?
beta blockers may mask the symptoms of hypoglycemia so diabetics should monitor blood glucose more closely
beta blockers contraindications
bradycardia (may lead to primary heart block)
cardiogenic shock
overt cardiac failure
Atenolol (Tenormin)
beta blocker (beta one selective)
anti anginal agent
treats HF, HTN, stable angina, and acute MI
PO 1/day
excreted 50% renal, 50% feces not metabolized!
anticholinergic may decrease GI absorption
beta blockers drug interactions
digoxin (and other antidysrythmics that depress myocardial conduction may lead to AV block)
adverse effects of beta blockers
bradycardia and hypotension
dyspnea on exertion, fatigue, pulmonary cogestion, peripheral edema
classic symptoms of HF
Why are ACEIs (or ARBs) a preferred drug in the treatment of HF?
ACEIs block the detrimental effects of angiontensin II and aldosterone on cardiac remodeling
Nesiritide (Natrecor)
has a limited role in HF treatment; ANP and BNP (Natrecor is BNP) cause diuresis, vasodilation, and decrease aldosterone secretion. Basically, Natriuretic peptides counteract the RAAS and SNS
give to patients with acutely decompensated heart failure
Patients at high risk for HF
make lifestyle changes
treat and control HTN, dyslipidemia, and diabetes
if htn, start ACEI
Patients with structural evidence of heart diseaes (MI or valvular disease) but no symptoms of HF
lifestyle, control of modifiable factors (HTN, lipids, diabetes)
ACEIs (ARBs)
Beta blockers if prior HF symptoms
Diurectics and salt restriction if fluid retention
Patients with structural evidence of heart disease with symptoms of HF such as fatigue, fluid retention, dyspnea
ACEI (ARB) and Beta Blocker
Add Digoxin and Spironolactone if needed to control sympotoms
If symptoms do not improve, add a loop or thiazide diuretic and a combo nitrate with hydralazine
3 goals of Pharmacotherapy of HF
reduce preload reduce afterload (reduce vascular resistance-BP) Inhibit RAAS and SNS (which are vasoconstrictors)
adrenergic blockers for HF
Carvedilol
decrease cardiac worload by slowing the HR (B1) and decreasing BP (alpha 1)
Vasodilators for HF
isosorbide dinitrate with hydralazine
decrease cardiac workload by dilating blood vessels and reducing preload
ACEI and ARBs for HF
lisinopril, captopril
increase cardiac output by lowering BP and decreasing blood volume
Phosphodiesterase Inhibitors for HF
Milrinone
increase cardiac output by increasing the force of myocardial contraction
Cardiac glycosides for HF
Digoxin
increase CO by increasing the force of myocardial contraction
Main ACEI adverse effects
hypotension (worse at beginning of treatment and when dose is changed) caution with Beta blockers and diuretics
renal insufficiency resultant of decreased blood flow or hyponatremia from diurectics
angioedema, cough, hyperkalemia
What is a risk associated with ACEI + spironlcatone?
hyperkalemia
Losartan (Cozaar)
ARB used for HF when ACEI is not tolerated
Diurectics Action
reduce peripheral edema reduce pulmonary congestion reduce blood volume reduce BP reduce cardiac workload INCREASE CO **only use diuretics in HF pts if fluid retention is present
Can you give loop diuretics to pts with renal insufficiency?
yes
examples of loop diurectics
furosemide (Lasix)
bumetanide (Bumex)
torsemide (demadex)
What diuretic is prescribed for mild-moderate HF and can be combined with loop diuretics?
Thiazide diuretics: chlorotiazide (Diuril), hydrochlorothiazide (HCTZ, HydroDIURIL)
Spironolactone (Aldactone)
potassium sparing and aldosterone antagonist diuretic
limited efficacy in HF pts bc low performing diuretic
blocks cardiac remodeling of aldosterone
when is it best to give ACEI for HF
within 36 hrs of onset
Diuretic cautions
dehydration and electrolyte imbalances
weigh self frequently
electrolyte tests (hypokalemia loop or thiazide especially when combined with digoxin)
If beta blockers, being negative inotropes, make HF worse, then why do we prescribe them to HF patients?
Beta Blockers stop the SNS compensatory response that makes HF worse and is a vicious cycle by blocking NE and other catecholamines that cause cardiac remodeling and disease progression. The result of beta blocker therapy is reduced HR and BP which leads to decreased cardiac workload.
After several mos of therapy, heart shape, size, and function can actually return to normal-> reverse remodeling
Which medication can cause reverse remodeling in HF patients?
beta blockers, carvedilol (Coreg) and metoprolol (Toprol), propranolol (nonselective)
How must beta blockers be administered to HF patients?
To prevent making HF worse, beta blockers must be given very specifically:
Initial doses must be 1/0-1/20 target dose and then doubled every two weeks until target dose is reached.
Beta Blockers are contraindicated for
COPD
bradycardia
heart block
beta blockers are used with caution on pts with
PVD, diabetes, or hepatic impairment
What lab tests do you monitor for pts on beta blockers?
liver function studies for signs of toxicity
How do vasodilator reduce symptoms of HF?
Vasodilators reduce preload or afterload
Hydralazine with isosorbide dinitrate
vasodilators: relax blood vessels and lower bp creating less workload for the heart;
use is limited due to risk of orthostatic hypotension and reflex tachycardia
Hydralazine
antiHTN acts on arterioles to decrease peripheral resistance, reduce afterload, and increase CO; not a first choice drug bc of hypotension and reflex tachycardia risks
Isosorbide Dinitrate
a long acting organic nitrate that reduces preload by directly dilating veins. not effective as monotherapy and tolerance develops quickly
what triggers the release of BNP in the body?
increased ventricular stretch releases BNP which then enhances diuresis and renal excretion of sodium (counteracts RAAS and aldosterone)
Patients with acutely decompensated heart failure are prescribed which vasodilator?
Nesiritde (BNP) and monitor this patient continuously bc hypotension may occur
What drug do you give to patients with supraventricular tachyarrythmias (afib)?
Digoxin-now a drug reserved for late stage HF
digoxin has antidysrythmic properties
Why are cardiac glycosides used in late stage HF only?
they have a narrow therapeutic window and severe side effects
When do you hold digoxin?
when HR is <60bpm
Two Primary classes of positive inotropic agents administered to pts with acute decompensated HF:
Beta AGONISTS
Phosphodiesterase Inhibitors
Beta Agonists
isoproterenol (Isuprel)
EPI, NE, Dopamine
Dobutamine (Dobutrex)** ability to rapidly increase myocardial contractility with min changes to HR and BP
two common adverse effects of beta agonists
tachycardia and dysrythmias
When do you give dopamine in HF?
when the pt has both HF and hypotension bc dopamine can increase myocardial contractility and activates alpha receptors to increase BP
How do phosphodiesterase III inhibitors work?
they block the enzyme which leads to increases in the amount of calcium available for myocardial contraction. Two benefits:
positive inotropic and vasodilation, thus CO is increaseed due to increased contractility and decreased in left ventricular afterload. There is little effect on HR
Prototype drug for phosphodiesterase III inhibitor
milrinone (Primacor)
ACEI action r/t HF
Lower peripheral resistance through inhibition of angiotensin II formation
reduce blood volume through inhibition of aldosterone
yields reduced arterial BP (afterload), increased CO, and dilated veins (preload)
digoxin action (4)
decreases SNS activity and increases PNS activity-can suppress SA node and slow conduction through AV node;
inhibits NaKATP Pump
increases intracellular calcium via sodium/calcium exchange pump
positive inotrope; by increasing mycardial contractility, digoxin increase CO and that improves exercise tolerance and urine production to restore fluid balance and decrease pulmonary congestion.
special considerations when administering digoxin
must give over a min of 5 mins, can dilute in 4-5mL
can give PO but NEVER IM or SC
Is digoxin highly protein bound?
Yes, so be aware of hypoalbumuria-toxic dig
Adverse effects of digoxin
ventricular dysrhythmias including sudden cardiac death. most common cause is hypokalemia from combined diuretic therapy; hypomagnesemia and hypo calcemia and impaired renal function are add’l risk factors. AV Block, atrial dysrhythmias, sinus bradycardia
Normal serum digoxin levels
0.5-1.5ng/dL drawn 6-12 hrs after last dose
toxicity often presents with flu like symptoms/ earliest sign is anorexia
H2antagonist
antagonist agent against histamine that decreases gastrin secretion
cathartic
agent with purgative action
Rapid, intense fluid evacuation of bowel.
surfactant
a surface active agent also known as a wetting agent, tension depressant, detergent and emulsifier
Methoscopalamine
blocks effect of Ach and relaxes smooth muscles
GI Stimulant
adjunct therapy for treating peptic ulcer disease
Dexpanthenol
minimizes risk of paralytic ileus when used post op
metoclopramide PO meal consideration and what does it treat?
take 30 mins before meals and at bedtime
dopaminergic blocker
treats v/n, and expedites gastric emptying
metoclopramide IV considerations
give 30 mins prior to chemo for antiemetic effect
GI stimulants
decrease reflux by increasing sphincter tone and enhancing acid clearance and decreasing gastric emptying.
Used for delayed gastric emptying caused by diabetic gastroparesis, GERD, or post op N/V
Stimulates gastric mobility w/o stimulating gastric, biliary, or pancreatic secretion
GI Stimulants contraindications
Hx seizure d/o, pheochromocytoma, PD (metoclopramide)
GI hemorrhage, obstruction or perforation
allergy to dextran, CHF, renal failure (dexpanthenol)
depression, HTN
nursing considerations for GI stimulants
monitor for possible hypernatremia and hypokalemia paricularly if pt has CHF or liver cirrhosis
monitor BP closely with metoclopramide IV
Client edu for GI stimulants
report signs of acute dystonia immediately
do not drive a few hours after taking metoclopramide
avoid humid environments with methoscopolamine
Anticholinergic and Antispasmodics
medications for decrease GI tone and motility
pylorospasm, ileitis, and IBS
give 30-60 mins before meals and at bedtime
Anticholinergic and Antispasmodics Contraindications
narrow angle glaucoma, obstructive GI disease, paralytic ileus, obstructive uropathy, adhesions between iris and lens, myocardial ischemia, and toxic megacolon.
Caution if renal dysfunction
Atropine may increase the effect of
phenothiazines
increased effects of atenolol with
anticholinergic drugs
what decreases absorption of anticholinergics
antacids
Cytotec (Misoprostol) contraindications
contraindicated if allergic to prostaglandins, pregnant, or lactating. May cause spontaneous abortion.
Prostaglandin Analog
Misc drug for PUD/GERD: Misoprostol (Cytotec)
protects against peptic ulcers caused by NSAIDS by reducing the secretion of gastric acid and by boosting the production of gastric mucus
Is a prostaglandin Analog
Carafate (Sucralfate)
butt paste; works locally in the stomach by rapidly reacting with Hcl to form a thick, paste-like substance that adheres to the gastric mucosa to form a protective acid resistant shield in the ulcer crater. In addition, stimulates prostaglandins, mucus, and bicarb; Protects the mucosa for up to 6 hrs
indicated for short term therapy, esp to treat ulcers r/t stress
**Not effective for ulcers r/t NSAIDS
Carafate (Sucralfate) danger
can result in aluminum toxicity in renally compromised patients when combined with aluminum salt antacids
carafate (Sucralfate) administration
1 hour before meals or 2 hours after meals; 2 hours after other po meds and not within 2 hours of antacids
cytotec nursing considerations
Pregnancy test prior to starting Cytotec and should be negative within 2 weeks of starting. Use contraception while on the med and for at least 1 month after stopping.
Cytotec take on empty stomach and not within 30 minutes (before or after) food intake
opioid related drugs, kaolin and pectin (in bananas) to treat diarrhea
Decrease peristalsis in the intestines. Include: Difenoxin Diphenoxylate with Atropine (Lomotil)* Loperamide (Imodium)- is an analog of Demerol
which opioid related drug treats long term diarrhea?
Loperamide is also used to treat chronic diarrhea
opioid related drugs adverse effects
GI distress
Lomotil- dizziness, lethargy, drowsiness; at high doses the anticholinergic effects may be observed (drowsiness, flushing, dry mouth & tachycardia); additive effects with other CNS depressants
antidiarrheal agents
paregoric/opium tincture diphenoxylate (Lomotil®) defenoxin (Motofen®) loperamide (Imodium, Kaopectate®) bismuth subsalicylate (Pepto-Bismol) Octreotide acetate (Sandostatin)- profuse watery diarrhea, severe diarrhea associated with metastatic tumors
nursing indications of antidiarrheals
Do not give to clients with C. difficile
Typically do not use to treat diarrhea in children.
Avoid bismuth subsalicylate if allergic to aspirin. This medication may temporarily darken stools and tongue.
kaolin and pectin
Pharmacodynamics:
Bind with bacteria, toxins, and other irritants on the intestinal mucosa.
Pectin decreases the pH in the intestinal lumen which provides a soothing effect on the irritated mucosa.
Pharmacotherapeutics:
Used to relieve mild to moderate diarrhea.
osmotic laxatives
Work by drawing water into the intestine promoting bowel distention and peristalsis. Include the following drugs: Glycerin (Glycerol) Lactulose (kristalose) Polyethylene glycol (Miralax) Saline compounds
PUD lifestyle treatments
Lifestyle changes Stop tobacco use Stop ETOH Stop Caffeine Weight control Decrease use of NSAIDS, ASA*
PUD drug therapy
Aimed at either eradicating H. pylori or restoring balance between acid and pepsin secretions and the GI mucosal defense.
These drugs include: systemic antibiotics, antacids, Histamine-2 (H2)-receptor antagonists, proton pump inhibitors, and other peptic drugs such as misoprostol and sucralfate.
H2 Blockers
BLOCK the release of hydrochloric acid in the stomach in response to gastrin "Tidines" cimetidine (Tagamet®) ranitidine (Zantac®)* famotidine (Pepcid®) nizatidine (Axid®)
Antacids
Interact with gastric acids at the chemical level to neutralize them
are inorganic compounds that contain aluminum, magnesium, sodium, or calcium to neutralized gastric acid and inactivate pepsin. They stimulate prostaglandin production and increase LES tone (reduces GERD)
therapeutic levels must increase stomach acid to at least 3.5
PPIs
Suppress secretion of hydrochloric acid into the stomach lumen
*Drugs of choice for PUD/GERD
Omeprazole (prilosec)
“prazoles”
bind irreversibly to enzymes that produce Hcl-long acting
take 2–30 mins before breakfast
no renal clearance (ok to give to pts with renal insufficiency)-metabolized in liver, excreted in urine/feces
long term therapy increases risk for osteoporosis (decrease calcium absorption)
other PPIs
Esmomeprazole (Nexium)
lansoprazole (prevacid)
pantoprozole (Protonix)
rabeprazole (AcipHex)
anticholinergics: Pirenzepine (Gastrozepine)
Misc drug for PUD/GERD
Reduce gastric motility
Adverse effects of dry mouth, constipation make this rarely prescribed now.
Mucosal barrier protectants
Coat any injured area in stomach to prevent further injury from acid
Lactulose (kristalose)
osmotic laxative
given in renal disease too
pulls amonia into gut and you poop it out
H2 Blockers Indications
PUD GERD Reflux esophagitis Prevention of aspiration pneumonia Prevention of stress ulcers in critically ill clients, and as combination therapy to treat H pylori infection
H2 Blockers Nursing considerations
Avoid antacid use within 1 hour of po administration.*
IV preparations should not be mixed with other medications.
Once a day dosing should be at bedtime; more often five before meals.
Use cautiously in clients with renal or hepatic function impairment.
PUD
the incidence of PUD is associated with the following risk factors:
H. pylori infection
Family hx of PUD
corticosteriods, NSAIDS, ASA, platelet inhibitors
Blood group O (H. pylori may bind to this antigen)
Smoking tobacco
excessive caffeine
stress
NSAID related ulcers are usually where? (PUD)
gastic ulcers
less common
anorexia, weight loss, vomiting
H. pylori related ulcers are usually where? (PUD)
duodenal ulcers
gnawing or burning upper abdominal pain that occurs 1-3 hrs after a meal. Pain is worse in empty stomach and often disappears with ingestion of food. (presence of food closes the sphincter and keeps acid in stomach) red vomit, black tarry stools.
what contributes to stress ulcers? (PUD)
vasoconstriction secondary to SNS involvement causes decreased blood flow to small intestine
ZES (Zollinger-Ellison Syndrome)
less common cause of PUD
caused by a tumor that secretes gastrin (gastrin increases Hcl secretion)
results in too much acid
GERD
persistent Heartburn, dysphagia, dyspepsia, chest pain, nausea, belching
symptoms worsen following large meals, exercise, and when reclining
What makes GERD worse?
caffeine, alcohol, citrus fruits, tomato based products, onions, carbonated beverages, spicy food, chocolate, smoking, pregnancy, and obesity
Which meds make GERD worse?
nitrates, benzodiazepines, anticholinergics, beta blocker, alpha blockers, estrogen, progesterone, iron, CCBs, NSAIDS, tricyclic antidepressants, opioids, levodopa, biposphonates, and some chemo agents
Warning s/sx of GERD
unexplained weight loss, early satiety, anemia, vomiting, initial onset of symptoms after age 50, prolonged anorexia or dysphagia
Goals of PUD pharmcotherapy
provide immediate relief, promote healing of ulcer, prevent complications, prevent future recurrence
for PUD patients with H. pyloria
antibiotics are key to pharmacotherapy
Drugs to provide relief for PUD/GERD
neutralizing gastric acid PPIs H2 blockers Antacids *long term acid suppression leads to deficiency in folic acid, iron, and vit B12**
H2 blockers
"Tidines" cimetidine (Tagamet) famotidine (Pepcid) nizatidine (Axid) ranitidine (Zantac)
Sodium antacids disadvantages
avoid if sodium restricted diet or have HTN, HF, and renal impairment bc they cause fluid retention
Magnesium antacid disadvantages
hypermagnesemia (fatigue, hypotension, dysrhythmias)
laxative effect in large intestine
Calcium antacid disadvantages
constipation risk and may cause/aggravate kidney stones
hypercalcemia, renal failure at high doses
calcium carbonate antacids with milk or vit D can cause milk-alkali syndrome
s/sx of hypercalcemia and milk-alkali syndrome
HA, urinary frequency, anorexia, nausea, fatigue
Aluminum antacids disadvantages
constipation
aluminum carbonate and aluminum hydroxide may interfere with dietary phosphate absorption to cause hypophosphatemia
bicarb antacid disadvantages
may provoke metabolic alkalosis (fatigue, mental status changes, muscle twitching, depressed RR)
bicarb combines with gastric acids to form CO2-causes bloating and belching
drug interactions with antacids
increase stomach pH-affect solubility and absorption of many PO meds
acidic drugs will have a lesser therapeutic effect and basic drugs will have a more intense effect
enteric coated or delayed release drugs are designed to dissolve in the alkaline environment of the small intestine-antacid use may cause these drugs to dissolve early in the stomach and the drug may then irritate stomach lining
antacids bind to tetracyclines and digoxin
by changing urine pH, antacids delay the elimination of basic drugs (amphetamines) and speed the elimination of acidic drugs (aspirin)
Acidic drugs
NSAIDs, sulfonylureas, salicylates, warfarin, barbiturates, isonizaid, digoxin (decreased action with antacid)
basic drugs
morphine sulfate, antihistamines, tricyclic antidepressants, amphetamines, quinidine (increase action with antacid)
To decrease potential for antacid-drug interactions, what should the nurse advise her patients to do?
other meds should be taken at least 1 hour before or 2 hours after an antacid
Pharmacotherapy of H. Pylori
Omeprazole (PPI), clarithromycin (Biaxin), amoxicillin
or add metronidazole (Flagyl), bismuth subsalicylate (peptobismol) and tetracycline
how does bismuth compound work to treat H pylori?
inhibit bacterial growth by disrupting cell walls and prevent h pylori from adhering to gastric mucosa
how do PPIs treat h pylori?
suppress h pylori, and the increased pH creates a hostile environment for H pylori, thus enhancing effectiveness of antibiotics
Misc drug for PUD/GERD: bismuth compounds (Kaopectate or PeptoBismol)
contains both bismuth and salicylate which stim mucosal bicarb and prostaglandin production and inhibits H pylori from adhering to ulcerated tissue. causes cell wall death to h pylori.
turns stool black-normal side effect
childrens pepto
contains calcium carbonate but no salicylates due to increased risk of developing Reye’s syndrome with salycylate use under age 19
Misc drug for PUD/GERD: Metoclopramide (Reglan)
more commonly prescribed to treat n/v associated with chemo, but used for PUD/GERD when pts dont respond to first line drug therapy
Causes muscles in the upper intestine to contract, resulting in aster emptying of the stomach
Decreases esophageal relaxation and blocks food from entering the esophagus (GERD benefit)
adverse effects of metoclopramide (Reglan)
drowsiness, fatigue, confusion, insomnia
uncommon: parkinsonism (bradykinesia, akathisia, and tardive dyskinesia)
which two antacid compounds may cause constipation?
aluminum and calcium antacid compounds may cause constipation
Sodium compounds may cause flatulence
Magnesium compounds may cause diarrhea
What adverse effects should a nurse monitor for in pts taking ranitidine (Zantac)?
blood dyscrasisas have been reported, especially neutropenia, and thrombocytopenia so the nurse should performed periodic blood counts
Bulk forming laxatives
calcium polycarbophil (FiberCon, Equalactin)
methylcellulose (Citrucel)
psyllium mucilloid (Metamucil, Naturacil)
absorb water, thus adding to the size of fecal mass (the larger the fecal mass, the greater the neural stimulus for defecation)
take with plenty of water or you could obstruct your esophagus!!
Bulk forming laxatives are the treatment of choice for chronic constipation and may be taken on a regular basis without ill effects.
Stimulant laxatives
bisacodyl (Correctol, Dulcolax)
castor oil (Emulsoil, Neoloid)
promote peristalsis by irritating the bowel; rapid acting and more likely to cause diarrhea and cramping than bulk forming laxatives.
do not use frequently: laxative dependence, abdominal cramping, and fluid/electrolyte imbalances may occur
used as a bowel prep prior to bowel exams/surgeries
Surfactant laxatives / stool softeners
docusate (Colace)
cause more water and fat to be absorbed in stool
ineffective in treating constipation but are most often used to prevent the condition.
Saline/Osmotic Cathartics magnesium hydroxide (Milk of Magnesia) polyethylene glycol (MiraLAX) sodium biphosphate (Fleet Phospho-Soda) Glycerin (Glycerol) Lactulose (kristalose) Saline compounds
pull water into the fecal mass to create a more watery stool
can produce a BM very quickly
do not use long term due to risk of dehydration and electrolyte depletion
Saline laxatives are important for colonoscopy prep or for purging toxins from body
mineral oil as a laxative
should not be used bc it interferes with absorption of fat-soluble vitamins
opioids are the most effective drugs for controlling
severe diarrhea (codeine, Difenoxin
or diphenoxylate with atropine (Lomotil)*
caution use with MAOIs (hypertensive crisis may ensue)
loperamide (Imodium)
analog of meperidine (Demerol)
antidiarrheal agent
no analgesic actions, no issues with dependence
what do you administer to counteract an od of Lomotil (opioid)?
Naloxone
Ocreotide (Sandostatin) as an antidiarrheal
treats severe diarrhea associated with cancer
prevents release of serotonin and other active peptides that promote diarrhea; directly inhibits intestinal secretions and enhances absorption
long term therapy usually causes gallstones or cholestatic hepatitis
Treat IBS with
immunosuppressants and anti-inflammatory drugs
- 5-ASA (sulfasalazine, olsalazine, balsalazide, mesalamine)
- oral coritcosteriods (prednisone)
- (Immunosuppressants) azathioprine (Imuran), mercaptopurine (Purinethol), methotrexate- onset 3 mos effective at expanding time between relapses
- TNF inhibitor (Remicade), adalimumab (Humira)
Budesonide (Entocort-EC)
corticosteriod that is first line for treatment of IBS bc it is encapsulated so it is not absorbed in stomach or duodenum (not GI irritation)
Drug is slowly released and reaches a high concentration in the terminal ileum and proximal colon (2 most affected sites for IBD)
almost entirely removed by liver in first pass metabolism-nill on side effects
treat n/v with
antiemetics
- cannabinoids
- serotonin blockers (antipsychotics)
antihistamines and anticholinergics
antacids
herbal supplements peppermint, ginger
Phenothiazines: prochlorperazine (Compazine), metoclopramide (Reglan), perpehenazien (Phenazine, Trilafon)
treat psychoses and antiemetic
EPS are a concern with long term therapy
Benzodiazepines lorazepam (Ativan)
anxiety and antiemetic
Cannabinoids dronabinol (Marinol)
like marijuana
Corticosteriods dexamethasone (Decadron) and methylprednisolone (Solu-Medrol)
prevent chemotherapy induced and post surgical n/v
serotonin (5-HT3) receptor antagonists: dolestron (Anzemet), granisetron (Kytril), ondansetron (Zofran)
most widely prescribed for treating n/v induced by chemo
Pancrelipase (Creon, PAncreaz, Zenpep)
used as replacement therapy for patients with pancreatitis or cystic fibrosis
The client who is taking sulfasalazine (Azulfidine) develops a sore throat, bruising, and severe fatigue. The nurse determines that the client is most likely experiencing drug induced
blood dyscrasias
The nurse teaches the client taking procholperazine (Compazine) to dc the medication immediately if what occurs?
facial twitching, tremors, muscle spasms, pacing
A nurse should question the order for pancrelipase for a client
with a pork allergy
A healthcare provider orders magnesium hydroxide (Mil of Magnesia) for a client with constipation. Before administering the drug, what should the nurse assess?
bowel sounds to make sure no obstruction
drugs used for weight management affect
appetite or the absorption of fats
lipase inhibitors (Orlistat/Alli/Xenical) cause weight loss
by interfering with the absorption of fats
indicated for those with BMI>30
only effective if taken with meals containing lipids; omit med if the meal has no lipid content
Anorexians
drugs used to induce weight loss by suppressing appetite and hunger
Lactulose
Lactulose is used to treat constipation and decrease ammonia* production and absorption from the intestines in liver disease.
Mineral Oil (lubricant laxative)
May impair the absorption of many oral medications such as fat-soluble vitamins (A,D,E,K ), oral contraceptives, and anticoagulants.
condansetron (Zofran®) antiemetic of choice in US
Doesn’t affect dopamine receptors, so no extrapyramidal effects*
absorbant drugs for OD treatment
Most commonly used adsorbent drug is activated charcoal.*
simple partial seizure
one hemisphere, manifestations include alterations in motor function, sensory signs, or sensory or autonomic symptoms
complex partial seizures
temporal lobe, may be preceded by an aura
impaired loc, repetitive, non-purposeful movements such as lip smacking, picking or aimless walking
amnesia is common
generalized partial seizure
both hemispheres
absence seizure
generalized, last 5-30 seconds, sudden cessation of motor activity and blank stare, can occur occasionally or up to 100x/day, eyelid fluttering and lip smacking, more common in children than adults
Tonic-clonic seizure
AKA grand mal
most common seizure
may be proceded by aura or have no warning
typically begins with loss of consciousness and sharp muscle contractions
pt falls to floor and may have urinary and/or bowel incontinence
breathing ceases and cyanosis develops during tonic phase
clonic phase follows with alternating muscle contraction and relaxation in al extremities, hyperventilation, eyes rolled back in head
postictal period: pt is relaxed with quiet breathing, unconscious, unresponsive, gradually regaining consciousness and may have transient confusion and disorientation
Diazepam (Valium)
Benzodiazepine
for seizures
most serious side effect is cardiovascular collapse; assess for hypotension, tachycardia, and edema
treat od with Flumazenil (Romazicon) reverses CNS depression
listed on Beers List of potentially inappropriate drugs for the older adult
hold drug if BP drops 20mmHG (orthostatic hypotension)
Assess respiratory status for depression (rate, rhythm, depth)
Phenytoin (Dilantin)
Hydantoin
prevents seizures (except absence seizures)
loading doses common; can be very toxic (nystagmus, confusion, ataxia, coma, seizures), monitor closely
gingival hyperplasia (use soft bristle toothbrush)
do not DC abruptly-risk for seizure
assess for blood dyscrasias (sore throat, bruising, nosebleeds)
Monitor serum glucose closely as Dilantin may inhibit insulin release-risk for hyperglycemia
therapeutic range of Phenytoin (Dilantin)
10-20 mcg/mL
Carbamezepine (Tegretol)
antiepileptic
risk for Stevens Johnson syndrome (fever, sore throat, fatigue)
treat OD with activated charcoal and gastric lavage
Valproic Acid (Depakote)
GABA Agonist
adverse effects of photosensitivity and pulmonary edema
treat OD with Naloxone (Narcan); hemodialysis can lower drug serum levels. Caution must be used when administering Narcan bc it can reverse the anitseizure action of Depakote
Therapeutic level of Valproic Acid (Depakote)
50-100mcg/mL
Muscle Spasm Medications
Carisoprodol (Soma) Cyclobenzaprine (Amrix, Flexeril) Diazepam (Valium) Metaxalone (Skelaxin) Methocarbamol (Robaxin)
Diazepam (Valium) uses besides seizures
anxiety, acute alcohol w/d, treat tetanus
Nursing considerations for muscle spasm meds
blood studies (CBC, WBC with differentials) assess for CNS depression, dizziness, drowsiness, and psychiatric symptoms
myasthenia gravis
occurs when antibodies attack nicotinic synapses on skeletal muscles resulting in symptoms of extreme fatigue, double vision, and difficulty chewing or swallowing. The most obvious symptom is ptosis. Diagnosis is accomplished by clinical symptoms and presence of antibodies to Ach.
Pyridostigmine (Reganol)
treats myasthenia gravis
Edrophonium (Tensilon)
diagnose Myasthenia Gravis; administer IV rapidly while observing pt repsonse. works 1x; toxic to liver and loses efficacy the more you use it
pyridostigmine (Reganol) side effects
severe cholingeric response (excessive salivation, sphincter relaxation, diarrhea, vomiting)
pyridostigmine (REganol) nursing considerations
assess repiratory
give w/ meals on time to keep in therapeutic range (short half live)
Levodopa and Carbidopa (Sinemet); Pramipexole (Mirapex); Benztropine (Cogentin)
treat parkinsons disease
levodopa and carbidopa (SInemet)
dopamine replacement agent
carbidopa makes levodopa more effective at smaller doses by inhibiting its breakdown in the intestine and peripheral tissues (more reaches brain); levodopa treats tremor, bradykinesia, gait and muscle rigidity
imbalance, sensory problems, sexual dysfunction and constipation do not respond well to levodopa
pramipexole (Mirapex)
dopamine receptor agonist
benztropine (Cogentin)
cholinergic antagonist
Dietary restrictions assoc with levodopa and carbidopa (SInemet)
avoid food high is pyridoxine (vit B6) (Beef, liver, ham, pork, egg yolks, whole-grain or fortified cereals, or multivitamins)-they will decrease medicinal effects
do not take with foods high in protein-neg effect on absorption
the full therapeutic effect of meds may take several months to appear
What’s another drug that is used synergistcally with levodopa to treat PD?
Pramipexole (Mirapex)
Watch for hallucinations, dizziness, drowsiness, and nausea
orthostatic hypotension
EPS (tongue rolling, confusion, jerking)
fainting, mood changes, muscle cramps/spasms, increased tremors, swelling of ankles/feet, chest pain, vision changes, dysrhythmias
BUN/cr
How do you combat EPS in Pramipexole drug therapy
pair with Cogentin (Benztropine)
adverse effects of Benztropine (Cogentin)
paralytic ileus, tachycardia, cardiovascular collapse, anaphylactic shock, can cause some psych conditions to worsen so monitor closely
Nursing responsibilities r/t Cogentin
use caution in hot weather, avoid using mechanical/heavy machinery (dizziness/drowsiness), avoid OTCs and alcohol
Alzheimers treatment
Donepezil (Aricept)
reversible cholinesterase that causes elecated Ach levels in the cortex, which slows the neuronal degradation of Alzheimers disease
adjust dosage no more frequently than q6wks
Donepezil (Aricept) Contraindications
DC if jaundiced urinary frequency and incontinence common A fib possible assess BP to hypotension monitor liver function studies
Patient education r/t Donepezil (Aricept)
report side effects of twitching, n/v/d, or rash
do not increase or decrease dosage abruptly
stop smoking
Sharp, stabbing, dull, aching-
nociceptive pain
Burning, tingling=
neuropathic pain
peripheral nociceptors analgesics
local anesthetics
Anti-inflammatory drugs
peripheral nerve analgesics
local anesthetics
Dorsal horn analgesics
local anesthetics, opioids, alpha2 agonists
brain analgescis
opioids, alpha 2 agonists
Endocet
oxycodone HCl + acetaminophen
norco
hydrocodone + acetaminophan
Percocet
oxycodone HCl + acetaminophen
Percodan
oxycodone + aspirin
Vicodin or Lortab
hydrocodone + acetaminophen
Vicodin HP
hydrocodone + acetaminophen
opium
morphine + codeine
activation of mu receptor
responsible for the analgesic properties of the opioids as well as some of the adverse effects such as respiratory depression and physical dependence (opioid agonists)
opioid agonist
activate both mu and kappa receptors
morphine, codeine
mixed opioid agonist-antagonist
occupy one receptor and block (or have no effect) on the other
pentazocine (Talwin)
butorphanol (Stadol)
buprenorphine (Buprenex)
Opioid Antagonist
block both mu and kappa receptors
naloxone (Narcan)
kappa binding only
analgesia, sedation, decreased GI motility
Mu binding
analgesia, sedation, decreased GI motility
respiratory depression, euphoria, physical dependence
**general actions of opioids
Analgesia Respiratory depression *Constipation (decrease GI motility) *Urinary retention *Cough suppression Emesis Increased ICP Indirect through CO2 retention Euphoria/Dysphoria Sedation Miosis Pupil constriction decreased Preload & afterload Watch for hypotension!
promethazine (phenergan)
ondansetron ( Zofran)
antiemetic drugs usually used to combat nausea/vomiting r/t opioid use
clinically used opioids for analgesia
fantanyl, morphine
clinically used opioids for cough suppression
codeine, Dextromethorphan
clinically used opioids Antidiarrheal
(Diphenoxylate,Loperamide)
clinically used opioids Acute Pulmonary edema
(Morphine)
clinically used opioids anesthesia
(Fentanyl)
clinically used opioids Opioid Dependence or adjunct in chronic pain
(Methadone)
highly effective opioids
fentanyl hydromorphone levorphanol meperidine methadone morphine oxymorphone **risk for respiratory failure!!
moderately effective opioids
codeine hydrocodone oxycodone percocet **Hepatotoxicity, respiratory depression, circulatory collapse, coma
opioids wit mixed agonist-antagonist effects
buprenorphine (mu agonist, kappa blocker) *resp depression
burorphanol (weak mu blocker, kappa agonist)
nalbuphine weak mu blocker, kappa agonist)
pentazocine (weak mu blocker, kappa agonist)
morphines respiratory depressive action may be used to treat
SOB assoc end stage cancer
HF
pulmonary edema
advantages of morphine therapy
no upper end dose limit and pts develop tolerance to all the adverse effects except constipation
morphine drug interactions
alcohol, skeletal muscle relaxants, MAOIs (increased sedation)
kava, valerian, chamomile (increase CNS depression)
St John’s Wort may decreased analgesic action
duramorph
a preservative free morphine sulfate commonl used for IV, epidural, and intrathecal use (PCA pumps)
nursing responsibilities for morphine
Nursing implications
Baseline vital signs (BP will be lower, RR, O2 sat, pain rating) monitor output (ensure no urinary retention), watch for falls, d/c all previous orders for pain meds, administer by micro-drip and infusion pump
Predetermined dose and lockout interval
hydromorphone (Dilaudid)
7-10 time effect of morphine
faster onset, but shorter duration of action
high abuse potential
hydrocodone
often paired with tylenol (Vicodin) or aspirin (Lortab)
increased risk of hepatotoxicity (no vicodin for pts with hepatitis)
Meperidine (Demerol)
duration of action is shorter than morphine
good for pts with GI pain (pancreatitis, biliary colic) *does not increase biliary tract pressure
Patients with pain and acute asthma
Less likely to produce histamine release
contraindications for meperidine (demerol)
Cautions/Contraindications
Neurotoxicity with sickle cell, burn injuries, or cancer
Severe/fatal reaction if given to patient taking MAOI
Produces a vagolytic effectincrease HR
In COPD may result in resp. depression
In increased ICP, may mask neuro parameters
If given IM, rotate sites as tissue irritation is common
Methadone
more potent that morphine
used for detox and maintenance programs
cautions: OTC drugs may potentiate action, orthostatic hypotension is common side effect and can last several weeks
**no euphoria prod by other opioids
oxycodone
pproximately 10 times more potent than codeine
Examples
Percocet, Tylox- with acetaminophen
Percodan- with aspirin
fentanyl
Brands
Sublimaze, Innovar, Duragesic
Uses
premed, with anesthesia, post anesthesia
Propoxyphene (Darvocet)
less potent that morphine Darvon (ASA) Darvocet (acetaminophen) not a good choice for older adults caution history of alcohol abuse
Butorphanol (Stadol) mixed opioid
Cautions:
hypertensive clients, contraindicated in MI ( cardiac workload), may increase CSF (monitor ICP)
Pentazocine (Talwin) mixed opioid
Caution
cardiac function
Nalbuphine (Nubain) mixed opioid
uses
preeop as adjunct to anesthesia; obstetric analgesia
opioids to avoid for older adults
Meperidine (Demerol), propoxyphene (Darvon),and pentazocine (Talwin) are more toxic in older adults and should be avoided
Diminished circulation, which results in slower absorption of IM or SQ drugs
Tramadol (Ultram)
centrally acting non opioid analgesic
no GI ulceration like NSAIDs
no respiratory depression of opioids
bind to pioid mu receptor (weak mu agonist) 10X<codeine
inhibits NE and serotonin reuptake in spinal neurons (inhibits pain transmission)
Tramadol adverse effects
vertigo, dizziness, HA, n/v, constipation, and lethargy
nervousness, tremor, anxiety, agitation, confusion, visual impairment, and hallucinations
seizures if also taking antidepressants
adjuvant analgesics
antidepressant (tricyclic antidepressants, SSRIs) for neuropathic pain
antiseizure (gabapentin [neurotonin], valproic acid [depakene], phenytoin [dilantin], carbamazepine [tegretol] for neuropathic pain
corticosteroids antiinflammatory; dexamethasone [decadron], prednisone [deltasone]
local anesthetics: Mexiletine [mexitil] antidysrhythmic for neuropathic pain; lidocaine [Xylocaine]
muscle relaxants: benzodiazepines for muscle spasms and anxiety; diazepam [Valium], lorazepam [Ativan], oxazepam [Serax]
meds to treat migraines
Ergot preparations Ergotamine tartate (Ergostat) Dihydroergotasmine mesylate (Migranal) **Sumatriptan (Imitrex) Antiseizure drugs Beta-adrenergic blockers Calcium channel blockers Tricyclic antidepressants
meds to treat tension headaches
Analgesics – ASA, acetaminophen, or ibufrophen
Muscle relaxants- amitriptyline (Elavil)
Anti-depressants with counseling
When giving pre-op sedatives/hypnotics to elderly patients
monitor closely for confusion or excitement and initiate measures to prevent injury or fall
First IV agents will be given, act within seconds
Then once patient is unconscious, inhaled agents will be given to maintain anesthesia
Inhaled agents are gases (nitrous oxide) or volitile liquids— prevent flow of sodium into neurons
Exact mechanism not known, likely that GABA receptors are activated
Not same mechanism of action as local anesthetics
agents administered to achieve balanced anesthesia
neuromuscular blockers
short-acting benzodiazepines
opioids
general anesthetics
IV meds first
promote relaxation, diminish pain, and promote sleep
Inhaled agents administered once IV agent has caused loss of consciousness
maintain anesthetized state
Malignant hyperthermia
triggered by all inhalation anesthetics except Nitrous oxide
characterized by muscle rigidity and profound elevation of temperature (109F)
risk is greatest when inhalation anesthesia is combined with succinylcholine, a neuromuscular blocker that can also trigger the reaction
Preanesthesia Agents
Benzodiazepines
Diazepam Valium
Midazolam Versed
Reduce anxiety, sedation, amnesia, “conscious sedation”
Preanesthesia Agents
Antihistamines
hydroxyzine [Vistaril]
sedation
Preanesthesia Agents
Opiod Analgesics
Morphine [Morphine] Meperidine [Demerol] Fentanyl [Sublimaze] remifentanil [ultiva] Sedation to reduce tension, anxiety, and to provide analgesia
Preanesthesia Agents
Phenothiazines
promethazine [phenergan]
Sedation, antihistaminic, antiemetic,decreased motor activity
Preanesthesia Agents
Anticholinergics
Atropine
glycopyrollate [robinul]
Inhibits secretions, bradycardia, vomiting, and laryngospasms
Preanesthesia Agents
GI Drugs
Ondansetron [Zofran]
Cimetidine [Tagamet]
metoclopramide [reglan]
Antiemetic
Decrease gastric acidity
Decrease stomach contents
Non anesthetic drugs nursing considerations
Physical assessment should include:
VS, reflexes, muscle tone and response, pupil size and reactivity, ECG, lung sounds, bowel sounds, affect and LOC
Monitor for:
HTN, tachycardia, prolonged apnea, bronchospasm, respiratory depression, paralysis, and hypersensitivity
If history is positive for hepatic or renal dysfunction, neuromuscular disease, fractures, myasthenia gravis, malignant hypertermia, glaucoma, or penetrating eye injury, the use of succinylcholine is contraindicated.
Propofol (Diprivan)
IV sedative-hypnotic used for induction and maintenance of anesthesia
Used to sedate patients undergoing mechanical ventilation or noninvasive procedures (endoscopy, radiation therapy, MRI)
Single injection onset 60 seconds and lasts 3-5 minutes; can be given low-dose continuous infusion
Adverse effects: respiratory depression, hypotension
Contains soybean oil, glycerin and egg lecithin (check for allergy); these are a great growth medium for bacteria- open and discard within 6 hours
Ketamine (Ketalar)
Causes sedation, immobility, analgesia and amnesia; responsiveness to pain is lost
Assessment-produces analgesia, amnesia and immobility, but not muscular relaxation
Increases secretions of the salivary and bronchial glands
During recovery, hallucinations, disturbing dreams and delirium may occur
Useful for young children* undergoing minor surgical and diagnostic procedures
anesthetics are usually combined with
EPI to decreaed systemic absorption and prolong the duration of action of the anesthetic and to promote local hemostasis.
caution used on end tissues (may cause tissue ischemia or necrosis) assess gag reflex if used in oral cavity
Use of vasoconstrictors, usually epinephrine, decreases local blood flow and delays systemic absorption and prolongs anesthesia and reduces risk of toxicity. If anesthesia absorption is slower, a lower dose can be used.
Local Anesthetics
Sodium Channel Blockers Classifications: Esters Cocaine procaine (Novocain) Benzocaine (Solarcaine) Amides lidocaine
If area has localized infection or abscess, tissue environment will be acidic and effectiveness of agent will be decreased—-
will add sodium hydroxide to neutralize environment
Amides
produce fewer side effects and usually have a longer duration of action
lidocaine (Xylocaine)
most commonly used amide for short surgical procedures
Ester-type anesthetics
(Cocaine, Novocain, Benzocaine) are metabolized in the blood by esterase enzymes.
Amide-type anesthetics (lidocaine)
are metabolized by enzymes in the liver.
