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Cardiovascular Medications
-Categories
antihypertensives
adrenergic
ACE inhibitors
ARB’s- angiotensin II receptor blockers
Ca Channel blockers
vasodilators
direct renin inhibitors
diuretics
antianginals
heart failure
anti-dysrhythmics
coagulation modifiers
antilipemic
diuretics
Adrenergic medications
-affect autnomic nervous system
parasympathetic- rest and relax
sympathetic- fight or flight
-affect sympathetic
stimulation (agnost)
increases HR (increased CO) at AV node
increased force of contraction (increases CO)
drives vasocontriction (increase SVR)
suppression (blockers/antagonist)
decreased HR at AV node (decreases CO)
decreased force of contraction (decreased CO)
drives vasodilation (decreased SVR)
RAAS System
-kidneys responsible for changes in BP
circulating blood volume associated with amounts of water and Na
-with drop in fluid/Na concentration: renin and angiotensinofen released into blood → angiotensin 1 → angiotensin 2 via ACE enzyme → stimulates vasocontraiction and increases aldosterone release → stimualtes ADH and Na+ reuptake
-ARB’s and ACE inhibitors affect this system
Antianginals
-potent- do not need a lot
SM relaxation in cell
reduce HR to reduce demand on heart
-Categories
nitrates and nitrites
beta blockers
Ca Channel blockers
ranolzaine
Heart Failure Categories
-Angiotensin-Convertin Enzyme (ACE) Inhibitors
-Angiotensin II receptor blockers (ARBs)
-Angeiotensin-receptor neprilysin Inhibitor (ARN’s)
-Aldosterone Antagonists
-Phosphodierterase Inhibitors
-Cardiac Glycosides
Antidysrhythmics
-correct abnormal electrophysiollogic function- correcting rate and rythmn
-effectiveness increases as number goes higher for class
Coagulation Pathophysiology
-can modify pathways to inhibit or enhance clotting pathways
-hemostasis- any process that rsults in the stopping of a bleed
-coagulation- when bleeding is stopped by a clot formation
-thrombus- clot
-embolus- clot on the move
-firbin- major component of thombi (made by fibrinogen)
-fibrinolysis- breakdown of fibrin/trhombi
-plasmi- breaks down firbin/thrombi
-Coagulation Derangement- excessive clotting, lack of fibrinloysis, inability to clot
CVA
DVT
MI
Exsanguination
Coagulation Modifiers
-anticoagulants- no blood congealing; prevent clot formation
ALWAYS QUESTION 2 ANTICOAGULANT ORDERS
-antiplatelets- stop platelet plug formation; prevent adherence of platelets to site to cuase the clot
-thrombolytics- help breakdown clots
-antifibrinolytics- stop clot breakdown so its stays where it needs to be
Anticoagullants transition
-for short transition from one medicaiton to another can be on two anticoagulants
-taper one and slowly raise the other to keep blood levels stable wihtout window of anticoagulation
4-5 day transition
prioritize therapeutic levels
Heparin Complications
-Heparin-unfractionated- large molecule that can have unpredicatble affect os need labs q6hr for clotting check
-Enoxaparin-fractionated- small molecule so more available in body and more stable throughout, longer half-life (stays in body longer)
HIT (Heparin Induced Therombocytopenia
-ie drug allergy to heparin medications
-signifcant drop in platelets that is either gradual or acute
-body form numerous clots and uses up platelets in that process
-worried about: strokes, PE, DVT
-check patients labs!
Types:
type 1- can keep doing therapy; gradual drop in platelets
-type 2- much worse, acute and fast drop in platelets (>50%); stop use of medication therapy
Nursing Considerations for Coagulation Modifiers
-assessment
bleeding risk
clotting risk
labs- PTT, INR, platelets
-administration
contraindications
dose
monitoring
-monitoring for
bleeding signs
signs of thrombus
labs- PTT, INR, PLT, CBC
-have caution when combining multiple coagulation modifiers (RED FLAG)
Antilipemic Drugs
-Cholesterol- fat soluble steroid in animal fats and throughout body
steroid hormones
cell memebrane
bile acids
-triglycerides
fatty acids and glycerl
storage of unused calories- released for energy
-Liver can make varying amounts of cholesterol and usually all that we need- builds up in system as we eat it
-risk of coronary heart disease in patients with cholesterol levels of 300 mg/dL is three to four times greater than that in patients with levels less than 200 mg/dL
want to reduce build up in blood vessels
-Primary- prevention of the first cardaic event
-Secondary- prevention of subsequent cardiac events
-Treatment
first options start with diet and exercise
increase herbal options- flax/seed, soy, green tea
Rhabdomylosis
-risk from antilpemic statin drugs
Muscle Breakdown → Myoglobinuria →Kidney damage → Kidney Failure
muscle break down and leaves via urine and hurts kidneys which can put them into failure
more common when combined with other meds that increase the risk
need to educate patients on this as it is deadly and can have mild s/s
-Increase Risk:
Specific drug combinations
Grapefruit juice
>65 Years of age
Hypothyroidism
Renal Insufficiency
-Signs/Symptoms:
Muscle Soreness
Changes in Color of Urine
Antilipemic Drugs- Bile Acid Sequestrants
-administration timing must be either 1 hour before or 4-6 hours after any other medications
allows correct absorption into GI tract
Diuretic Medications
-classes- based on site of action in nephron structure
carbonic anhydrase inhibitors
loop diuretics
osmotic diuretics
postassium-sparing diuretics
thiazide
thiazide-like diuretics
Diuretics- Nursing Assessment
-must include:
Auscultation of breath sounds and heart sounds
need to know baseline VS
thorough medical hx
Determining neurologic status (need to know baseline)
Moisture levels
capillary refill
Vital signs- want to be stable before giving
Postural blood pressures can drop 20mmHg when given
Weight- monitor for loss of fluid
Intake/output measurements
want patient in a deficit so that output > input
-Lab Values Associated- many medications do not work if kidneys are impaired and can cause further kidney damage
renal failure
BUN, Creatinine
hepatic function
ALP, ASP, LDH
serum electrolytes
Nursing Evaluation for Diuretics
-resolution or reduction in
edema
fluid volume overlod
heart failyre
HTN
intraocular pressures
-monitor patient for the occurence of adverse reactions
Diuretics Lifespan Considerations- Age Extremes
-Increased risk for adverse effects
for both young and old
-Taken in the morning to help prevent nocturia
as young and old have increased sensitivity to adverse effects, important
-Assess living arrangements
can do home health visits for monitoring and living arangements
to assess SE (dizzy, confusion, headaches)
-Thiazide diuretics
cross the placenta
avoid in pregnancy
-Half-life of furosemide is increased in neonates
stays in their body longer
Autonomic Nervous System
-sympathetic (SNS) → stress
adrenergic (PNS) → accelerate
catecholamines → neurotransmitters (epinephrine, norepinephrine, dopamine)
-parasympathetic (PNS) → peace
cholinergic → calm
Adrenergic Drugs: Vasoactive Adrenergics
-affect this equation
CO x SVR → BP
BP: increase HR and contractility → increase CO so the heart can push out more
SVR: (after load) increases BP (vasoconstriction)
-Vasoactive Adrenergics
Assess the IV site
vesicant- a medication that can cause severe damage to vessels and surrounding tissue (burns tissue when in contact with non-intravascular tissue)
concern for dopamine and midrodrine
-Adrenergic Blocking Drugs- block the SNS (stress)
classified based on adrenergic receptor they block
Alpha 1 and 2 and Beta 1 and 2 receptors
Adrenergic Drugs: Miscellaneous Medications
-respiratory meds
-nasal decongestants
-opthalmic medications
-overactive bladder
Mirabegron (Myrbetriq) (sustained release)
relaxes detrusor muscle (in pelvic floor to increase capacity to hold on to urine)
increases bladder storage capacity
no contraindications
SE: HTN, UTI, headache, n, dizziness
Cholinergic Drugs
-Toxicity- cholinergic collapse
circulatory collapse
hypotension
blood diarrhea
shock
cardiac arrest
-treatment- support and anticholinergic
-SLUDGE
sweating and salivation
lacrimation
urination
diarrhea
GI cramps and pain
emesis