CV Flashcards
Adverse effects of Hydrochlorothiazide (HCTZ)
hypokalemia, hyponatremia, hypochloridemia
hypotension, hypovolemia
can increase uric acid levels
Effects/uses of Mannitol
strong diuresis,
rapid volume excretion needed for increased: ICP and IOP, renal fxn preservation
Blood is hypotonic: meaning, what is given
meaning: low solutes in blood, fluid going into cells,
give: hypertonic fluids (3% or 5% NaCl, 10% dextrose water (D10W)
Blood is isotonic: meaning, what is given
meaning: blood = same as cells about 280-300
give: isotonic (NS (0.9%), D5W)
Blood is hypertonic: meaning, what is given
Meaning: blood has high solutes (>300), risk for cellular dehydration
give: hypotonic (1/2 NS 0.45% NaCl)
Potassium Salts: uses, AE
Use: hypokalemia
AE: rapid can cause cardiac arrest, can be irritating to veins
Magnesium Salts: uses, nursing considerations
use: hypomagnesemia
considerations: dilute and infuse slowly, monitor for s/s of hyperMg (less activity - breathing, HR, muscles)
Effects of ARBs and direct renin inhibitors (remember they work in slightly different ways)
decreased vasoconstriction
increased Na+/H20 excretion and K+ retention
Decreased CV remodeling
AE of ARBs and Direct renin inhibitors
hypotension, dehydration, hyperK+
cough (less than ACE)
angioedema
fetal injury
AE of nondihydropyridines
constipation, dizziness, facial flushing, head ache, edema
bradycardia, heart block, decreased contractility –> decreased CO
drug interactions with nondihydropyridines
beta blockers
digoxin
AE of dihydropyridines
flushing, dizziness, HA, peripheral edema, increased myocardial O2 demand
drug interaction with dihydropyridines
beta blockers
AE of Hydralazine
SLE like syndrome, HA, dizziness, fatigue r/t hypotension
Drug interactions with nitroglycerin
hypotensive drug effects can be intensified
Contraindicated w/ PDE5 inhibitors
Caution w/: BB, calcium channel blockers, diuretics
What class are Quinidine and procainamide
class Ia antidysrhythmic
use of class Ia antidyrthmics
atrial and ventricular arrhythmias
AE of class Ia antidysrhythmics
anticholinergic (interact with M receptors)
What class is lidocaine
IB antidysrhythmic
Indications for lidocaine
post MI and other ventricular arrythmias
Uses of Class IC antidysrhythmics
supraventricular tachycardia, and a fib
Can we give desmopressin (DDAVP) for hemophilia A? Why or why not? Describe the mechanism of action of the drug.
This drug releases factor 8 clotting factors from the vasculature into the blood, it can be given for hemophilia A because the issue is producing/releasing these factors, so it increases the amount of factor 8 in the blood. It is preferred for mild forms
Understand the general ACC/AHA guidelines for the management of blood cholesterol. (In general, I don’t need you to memorize little details).What is the purpose of these guidelines?
The purpose of the guidelines is how to decide who to treat and to what intensity they need to be treated. It separates patients into two categories (high and very high risk), and subdivides high risk by age to determine who should receive the most aggressive statins
Who should be screened
Who is at risk (ASCVD 10 yr risk assessment)
Treatment: lifestyle modifications + low/med/high drug therapy
How should your patient’s HMG-CoA reductase inhibitor dosing be adjusted with acute renal failure?
Their CK should be checked, if it is elevated (which it will be) the drug should be discontinued
Discuss HMG-CoA reductase inhibitors and myopathy. What are the s/s? What are the risks? What can happen in severe cases? How do you educate your patients to monitor for this?
s/s: aches, tenderness, weakness, can progress to myositis, with increased CK and K+
Risks: female, old age, low BMI, chronic liver or kidney disease, higher statin dose, CYP34A inhibitors, OATP1B1 inhibitors, specific genetics
Watch for s/s: measure CK upon start of therapy and again if symptomatic
What is the difference in mechanism of action between warfarin & heparin? Why do you think a patient would be prescribed one over the other?
Heparin works by binding anti-thrombin → suppresses fibrin mesh formation. Heparin works relatively quickly, and can only be given via IV or sub Q injection, so it is typically only given inpatient.
Warfarin inhibits activation of vitamin K so clotting factors 2, 7, 9, and 10 are decreased, leading to lessened clots (decreased fibrin formation). Warfarin can take a while to work, and is oral so it is a medication patients are sent home on to prevent future clots.
Name the 4 classes of antidysrhytmics and describe how they work
1 - na+ blockers
A = increase AP, ERF, QT interval
B = decrease AP, ERF
C= increase ERF only in AV node
2 - beta blockers
3 - k+ blockers, delayed repolarization, increased AP duration, increased ERP, prolongs QT,
4 - decrease HR, contractility, conduction thru AV node
Other
Adenosine - hyperpolarizes by opening K+ channel,
Digoxin - na+/k+ inhibitors, increasing ca2+, thus increased contractility,
Name the 4 classes of antidysrhythmics and what they are used for
1 - na+ blockers
A = Atrial and ventricular arrhythmias,
B = Post MI and other ventricular arrhythmias
C= SVT and afib
2 - beta blockers - SVT, VT, post MI
3 - Ventricular tachy
4 - SVT
Other
Adenosine - tachycardias where pt is unstable
Digoxin - heart failure and supraventricular dysrhythmias
What is the difference in mechanism of action between the nondihydropyridines and dihydropyridines? How does this difference alter their clinical effects?
dihydropyridines only affect the vasculature, can cause reflex tachycardia, contractility increase, while nondihydropyridines affect both the vasculature and the heart rate, decreased contractility and AV node conductivity
List 2 cardioselective beta blockers
metoprolol, esmolol
What are the effects of amiodarone
delayed repolarization, increased AP duration, increases ERP, prolongs QT
Which HCG reductase inhibitor (statin) would you not give to someone of Asian heritage
Rosuvastain
What is Fenofibric acid
delayed release preparation of fenofibrate, reduces VLDL
How are monoclonal antibody (PCSK9) inhibitors given
sub Q or IV Q2weeks bc long half life (11-20 days)
indications of Exogenous erythropoietic growth factors (Epoetin alfa, Darbepoietin alfa)
Anemia d/t kidney d. (decreased endogenous EPO)
Palliation of chemo induced anemia
anemia preoperatively (need to increase H/H for surgery (expected blood loss), usually given with an anti-coagulant
-grel
P2Y12 ADP agonists
-teplase
thrombolytics
-stim
leukopoetic growth factors
-dipine
dihydropyridines
-xaban
factor 10 inhibitors
-parin
anticoagulants that activate antithrombin (like heparin)
-sartan
ARB
-pril
ACE inhibitor
-fibr-
fibric acid derivatives
What is the half life of thrombolytics
5 mins
Which part of RAAS contributes to cardiac remodeling?
aldosterone
Drug that decreases CV M+M
a. nifedipine
b. amioderone
c. diltiazem
d. lisinopril
d. lisinopril because it is an ACE inhibitor
does sodium nitroprusside cause reflex tachycardia
no
Hypo/hyper kalemia with digoxin
hypo: toxic
hyper: subtheraputic
AE of methadone
Can cause prolonged QT –> torsades
EKG prior to administration
avoid admin if QT>500 msec
Difference between heparin and LWMH
because the molecules in LWMH are smaller, there is decreased protein binding and a much longer half life (slower liver clearance), meaning they do not require lab monitoring
Indications of heparin
rapid anticoagulation
open heart surgery or dialysis to prevent device coagulation
low dose sub q for DVT prevention
treatment of DIC
adjunct to acute MI
Indications for direct thrombin inhibitors
A fib
Tx DVT/PE
prevention of thrombosis
hip/knee replacement
Indications of aspirin
CVA, TIA, chronic stable angina, stents, acute MI
inflammation, mild-moderate analgesia, fever reduction, suppression of platelet aggregation
Uses of P2Y12 inhibitors
prevent stent thrombosis and thrombotic events
Uses of PAR1 antagonists
w/ aspirin/clopidogrel in reduction of thrombotic events
Indication of GPIIb/IIIa receptor antagonists
short-term to prevent ischemic events in those with acute coronary syndrome or undergoing PCI
alteplase is an exogenous factor of
tPA (tissue plasminogen activator)
Dosing of factor VIII and IX concentrate
by % increase in factor desired in body weight
AE of iron supplementation
GI disturbances (take with food and water)
leading cause of poisoning fatalities in kids
AE of B12 supplementation
hypoK+ due to erythrocyte prodxn
Difference between epoetin alfa and darbepoetin alfa
darbepoetin alfa has a slower clearance and a longer half life so it can be given less frequently
Uses of thrombopoetin receptor agonists
thrombocytopenia (idiopathic or with liver disease pre-op)
Contraindications of cocaine
avoid with preexisting CV (tachy, dysrhythmias, MI)
dosing of inhalation anaesthetics
minimum alveolar concentration (MAC), concentration in the lungs that produces immobility to painful stimuli in 50% of the pop
AE of inhalation anaesthetics
Malignant hyperthermia dose-dependent HR and cardiac depression
sensitization of depression of pharengeal reflex - aspiration risk
nausea and vomitting
Uses of propofol
low dose for sedation
ver high dose for anesthesia
Uses of ketamine
analgesia
dissociative anaesthesia
AE of ketamine
Psychologic rxns (hallucinations, bad dreams)
–> avoid stimulation
Uses of celecoxib
osteo and rheumatoid arthritis
ankylosing spondylitis
acute pain
contraindications of opioid agonist antagonists
since nalbutaphine and butorphanol can increase cardiac work, avoid in MI
AE of methylnaltrexone
abd pain, nausea, flatulence, diarrhea
contraindications of methylnaltrexone
GI obstruction
AE of Naltrexone
IM injection site rxn (can be severe)
rare: hepatotoxicity
Drug in the serotonin receptor agonist class
sumatriptan (-triptans)
Indication for serotonin receptor agonists (triptans)
first line for migraine termination
How do serotonin receptor agonists (triptans) work?
promote vasocontriction and supress CGRT release causing decreased inflamation
AE of triptans
chest symptoms (transient, not ischemia)
coronary vasospasm
teratogenic
contraindications for triptans
CAD
printmetals
pregnancy
drug interactions with anything that causes increase NE or seratonin (SSRIs/SNRIs, MAOIs, ergot alkaloids, other triptans)
How do seratonin 1F receptor agonists work?
block trigeminal ganglia pain transmission
no vasoconstriction
overall not well understood
Abortive drug therapies for migraines
asprin-like drugs
seratonin receptor agonists (triptans)
seratonin 1 F receptor agonists
ergot alkloids
Calcitonin gene related peptide receptor antagonist
Indication for ergot alkloids
second line for migraine attack termination
AE of ergot alkloids
N/V, weakness/myalgia, N/T, teatrogenisis
OD: egotism: ischemia d/t peripheral vasoconstriction causes necrosis
contraindications of ergot alkloids
sepsis, PVD, renal or hepatic disease
AE of Calcitonin gene related peptide receptor antagonist
minimal, some nausea and somnolance
nursing considerations for Calcitonin gene related peptide receptor antagonist
high fat meal can delay aborption by as much as 2 hours
Indications for Calcitonin gene related peptide receptor antibodies
- when given
risks
prevent migraines, sub Q once per month, risk for antibody formation
How is benzocaine different from other local anesthetics
benzocaine has the adverse effect of methemoglobinemia, so it is contraindicated in those under 2
How is cocaine different from other local ananesthetics
Cocaine in addition to blocking na+ channels, cocaine also blocks NE reuptake causing CNS and CV stimulation
What makes chloroprocaine different from other local anesthetics?
Chloroprocaine is special because it is not effective topically (injection only) and has a short duration of action
How do inhalation anesthetics reach their site of action? Where is their therapeutic site of action
They reach their site of action through the lungs (concentration, solubility, blood flow and ventilation all play a role in their absorption)
Their therapeutic site of action is the CNS
Go through each body system and describe the effects that opioid agonists have. How are these adverse effects managed? (i.e. cough suppression can be managed by teaching your patient to deep breath & cough at intermittent intervals to clear secretions & prevent PNA)
Constipation - fiber, fluid, activity, stool softener, laxative
Miosis – usually not a problem
Respiratory depression – monitor, if needed stop opiods and give narcan. Elderly, young and those with respiratory disease are especially at risk
Decreased heart rate – stand up slowly to help avoid and limit orthostatic hypotension
Urinary retention – monitor I/Os
Orthostatic hypotension – educate pts
Cough suppression – educate pts to breath deep and cough, auscultate for crackles
Euphoria, emesis, birth defects, tolerance, neurotoxicity
Why do we avoid ergot alkaloids & triptans together?
We avoid ergot alkaloids and triptans together because they can cause excessive vasospasm
What phramacologic measures can be used to treat heart failure
REDUCE PRELOAD (Diuretics ACEi, ARBs, aldosterone antagonists, Venodilation)
REDUCE AFTERLOAD (ACEi, ARBs, BB (controversial, use w/ caution), Arteriole vasodilators)
INCREASE INOTROPY (CONTRACTILITY) (Cardiac glycosides (digoxin), Dopamine/dobutamine (sympathomimetics)
How does sodium nitroprusside work? long term AE?
Sodium nitroprusside works the fastest and is given IV and works by decreasing both preload and afterload, decreasing O2 demand (and decreasing the resistance on the heart) and has minimal reflex tachycardia. For hypertension emergencies, renally eliminated over days
long term AE: Thiocyanate toxicity causing CNS effects
What are the differences between cardiac beta1 blocker action and cardiac calcium channel blocker action?
Calcium channel blockers cause arteriole vasodilation, while beta blockers cause decreased renin release. Both BB and nondihydropyridines decrease HR, AV node conductivity and decreased contractility
List absolute contraindications for nondihydropyridines
Drug interactions: beta blockers, digoxin
Don’t want to use with anything that would cause low contractility
Why does digoxin cause increased urine output?
Increased cardiac output = improved tissue perfusion = improved renal blood flow = more glomerular filtration = increased UOP!
