EXAM 2 Flashcards
Heart failure
(Pump failure)
The heart muscles (myocardium) weakens and enlarges causing decreased ability to pump the blood through the heart and into the systemic circulation.
Congested Heart failure
They have now become fluid volume overload (SOB, gain weight, edema) /
Compensatory mechanisms fail and the peripheral tissues and lungs become congested (fluid overload)
Left-sided heart failure
Left ventricle is not pumping
Pulmonary congested (SOB/shortness of breath), cough, oliguria (400ml output), weight gain
Right sided and left sided typically looks the same
Right-sided heart failure
Right ventricle is not pumping
Peripheral edema, jugular vein distention, and weight gain
They also can have pulmonary edema and crackles, fluid volume over load
Causes of Heart failure
- Chronic HTN (when the heart has to pump harder against the blood vessels that has high pressure in them. When the heart has to work harder, the heart grows
- MI (heart attack): causes damage to heart tissue
- Coronary artery disease (CAD)/atherosclerosis: that means that. The vessels that sits on top oF the heart are not feeding the heart muscles well; so if the heart is not getting enough blood flow into the muscle, then it will start to decline)
Valvular disease: stenosis of the valves; means the valves are tight and the heart has to work harder to push the blood through them; regurgitation means when the valves doesnt close all the way, now the blood flow goes back. So the heart has to pump harder and harder to push that blood forward
-Congenital heart disease
-Aging: as we get older, the heart has to work harder and harder to function
Not everyone gets HF when they get older.
Cardiac Glycosides
We use cardiac glycosides to help improve the contractility of the heart. Make the heart muscle contract more efficiently; they are considered +INTROPES. To increase cardiac output; we perfuse the tissues, & if we perfuse the tissues, our organs work better (in particular our kidneys). They are gonna slow the hR down,
3rd line treatment for pt with HF. /
Inhibit the sodium-potassium pump Increases intracellular sodium leading to increased influx of calcium Causing cardiac muscle fibers to contract more efficiently
Positive Inotrope Negative chronotrope Negative dromotrope Used when other modalities don’t control manifestations
**improve myocardial contractility improves cardiac, peripheral and kidney function due to Increased cardiac output Increased cardiac output decreases preload improving renal perfusion caused decreased edema and promoting fluid excretion
Ianoxin (Digoxin)
A cardiac glycoside
A 2nd line treatment for HF
Used for pt that had Atrial fibrillation/Aflutter rate control (Irregular & rapid Heart rate) or have a low blood pressure
Slows hr down and DOESNT decrease bp
(Ex: if someone has a rapid HR we need something that would lower their hr, but not their bp)
Route: PO/IV
Its a highly protein drug ; means it needs a protein to rest on, if it doesnt have a protein to rest on, they will have active meds floating around; will increase risk of toxicity. ; protein binding power 30%
Small therapeutic window 0.5-2.0ng/ml
When we start to see pts above 2.0, that is when we start to see some toxic side effects such as: bradycardia, anorexia (not eating), N/V, diarrhea, visual changes* (having yellow halos in their visions), confusion, delirium dysrhythmias (ventricular)
Antidote: digibind, ovine: helps reduce levels of digoxin.
Pregnancy category C
You need to Rember that it is excreted by the kidneys. So we may need to lower the dose if the kidney function is not good; can lead to toxicity & pts with thyroid disease alter the metabolism of digoxin so we need to decrease the dose in pt with hypothyroid.
Increases myocardial contraction, increases CO, which increases tissue perfusion and lower HR (decreases AV conduction decreasing HR)
Drug interactions: one of the things we worry about is when pts are on potassium wasting diuretics, they can lose potassium, if they are also on digoxin the digion can get absorbed more readily; which leads to toxicity if they have low potassium levs already. Check potassium levels first before administering.
- cortisones or steroids increases the loss of potassium as well; which increases toxicity
-antacids its gonna decrease the acidity in the stomach, which interferes with the absorption of digoxin. Best to separate the medications by at least an hour.
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Potassium loss diuretics and increase risk of digoxin toxicity Cortisone solution taken systemically (po,IV) increases hypokalemia increasing risk of toxicity Antacids decrease absorption, stagger doses
Digoxin Nursing considerations
We know that it will decrease HR, so check Hr before
Obtain apical pulse prior to administration
Assess for signs of toxicity (abuses, vomiting, bradycardia ect. )
Monitor digoxin level
Monitor potassium level (why? Low potassium means that increases the absorption of digoxin , which leads to toxicity)
Phosphodiesterase inhibitors
Increase cardiac output
Lower hr & bp; for CHF
Primacor (milrinone)
Inocor
These are + inotropes
Which increase tissue percussions.
**Can use in CHF an improve contractility which increase tissue perfusion, in particular to the kidneys, which will allow th kidneys to get the fluid off.. to help get rid of all of the edema that they are experiencing with CHF.
IV only
For about 24-72 hours (call in a cardiac “tune up”)
Because theses are cardiac select meds, we might see an increase in hr ; watch out for tachycardia. These meds also cause vasodilation, we have a balance act to make sure their bp doesn’t get to low, we are lowering their bp but need to make sure it doesn’t get too low.
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Primacor (milrinone) Inocor
Positive inotropes that increase stroke volume, cardiac output, vasodilation
IV only 48-72 hours Cardiac dysrhythmia may occur, monitor EKG
Vasodilators
Another agent for heart failure
Decrease venous blood return to the heart, decrease pre load/
**gonna open up the arteries so thats gonna help decrease the workload of the heart,so it doesnt have to work that hard. This will alos help the heart from filing too much (decrease preload)
Arteriolar dilators
Another agent for heart failure
Decrease after load (the heart doesnt have to pump header) increasing cardiac output, increased renal perfusion by dilating arterioles, improve circulation to muscles. ;
ACE inhibitors
Another agent for heart failure
Dilate venues, arterioles, improve renal blood flow, decrease blood fluid volume. Certain ARBS also (Diovan, Atacand)/\
Help improve renal blood flow
Diuretics
Another agent for heart failure
We know we can use to get extra fluid off then have better fluid balance. When there’s better fluid balance, the heart can pump efficiently.
Aldactone (spironolactone)
Another agent for heart failure
Its a potassium sparing diuretic
We use in pts with HF especially low ejection fraction hf.
Blocks the secretion of aldosterone causing decrease fluid retention.
Beta- blockers
Another agent for heart failure
As long as pt doesnt have decompensated HF we can use. Bb will help heart work more efficiently.
Natrecor
Another agent for heart failure
Inhibits ADH (prevents body from holding on to extra fluid) help with vasodilation, diuresis (Acute CHF),
BiDil (hydralazine and isorbide dinitrate) :thats a meds that help them with getting renal blood flow or blood flow to the kidneys to help get the fluid off .
Angina
Chest pain, tightness, radiating to left arm and or neck
Is when someone expernce chest pain (chest pain, burning). It means the heart is not getting sufficiently amount of blood flow, due to plague (ex: blood clot) being in the arteries or coronary spasm (arteries constrict and cause a temporally constriction of blood flow).
If restrict the blood flow in the arteries that are feeding the heart muscles, thats how it’ll get ischemia, which causes chest pain. (Then can lead to a heat attack.)
What are the 3 types of angina?
Classic (stable)
Unstable (preinfarct)
Variant (prinzmetal, vasospasm)
Classic (stable) Angina
Person knows what causes their angina; they can predict it.
Ex: person goes for a walk, gets to top of hill, he develops angina then he walk back home.
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Occurs with stress or exertion (physical effort)
Unstable (preinfarct) angina
Occurs frequently with progressive severity unrelated to activity.
Progresses
Ex: the man that walks to the top of the hill, if the angina starts to happen before he gets to the top of the hill, that means something changed, its unstable; its gotten worst. He feels dizzy, SOB while walking.
Basically change in the symptoms
Now, if someone suddenly develops angina anaad never experienced it before, it is unstable because they went form nothing to something.
Variant (prinzmental, vasospasm)
Occurs during rest.
Typically the most alarming kind, because it can send someone into cardiac arrest because we have sudden blockage in the heart, usually caused by a vasospasm.
Nonpharmacologic measures to control angina
- avoid heavy meals: helps decrease the pressure on the heart, especially at night.
- avoid smoking & vaping: every puff causes vasoconstriction; then lead to angina
- avoid strenuous exercise: when we know someone who has angina or cardiac disease, we dont want to over do it
- avoid extreme temperatures: avoid being outside in less than 40-degrees for 20mins or so …or in 80 degree or more..puts workload on the heart and causes damage (ex: shoveling snow should be avoided)
- avoid emotional upset
- rest and relaxation techniques.
Antianginal drugs
Increase blood flow by increasing O2 supply (vasodilation) or decreasing O2 demand/ decreasing the heart’s need for oxygen.
Three types of antianginals
Nitrates
Beta-blockers
Calcium Channel Blockers
Beta-Blockers
An antianginal
Decreases the heart’s need for oxygen and the heart work more efficiently ; which in turn decreases angina.
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Decrease workload, decrease O2 demands
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Beta-blockers as antianginal decrease heart rate and myocardial contractility, reducing O2 demands and reducing angina.
Most useful in stable angina
Taper dose to avoid reflex tachycardia and recurrent angina pain
Remember it lower HR, if someone has heart block and we give them a beta-blocker, it can slow the conduction even more, so we need to be careful.
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Avoid in 2nd and 3rd degree AV block
Calcium Channel blockers
An antianginal
Help decrease the workload and oxygen demand. Dilate those coronary arteries a lil bit to ease the angina
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Used to treat both variant and stable angina
Calcium blockers would dialate those arteries to prevent those spasms in variant angina.
Prevent spams help decrease oxygen cardiac demand
Decrease contractility
Decrease after load
Decrease PVR (peripheral vascular resistance) basically decreasing BP
Decrease workload of the heart
*Remember the two groups of calcium channel blockers. But Remember all of them will help with angina.
Nitrates
An antianginal
Reduce venous tone, increase vasodilation, decrease workload.
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Increase vasodilation and also lower blood pressure and lower preload; helps the heart work more efficiently
*Keep in mind that nitrates are potent dilators, so someone can have a rapid drop in their blood pressure
More info: dilate those coronary arteries on the heart and also dilate the arteries around the body and drop bp and decrease the work of the heart.
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cause generalized vascular and coronary vasodilation increasing blood flow to coronary arteries, reducing ischemia
Forms of Nitrates: sublingual (SL), IV, ointment, patch, PO
Nitroglycerin
A type of nitrate
An antianginal.
Sublingual
Nitroglycerin (SL) its 0.4mg and it is inserted underneath the tongue wait 5mins and if the pain doesnt relieve in 5 mins, can take another pill, and if it doesnt relieve in 5mins, can take a third pill. If the angina still there after 5mins, call 911.
Patients should NOT swallow it because GI will deactivate it.
The tablets should be kept in the dark and not exposed to the light
This is NOT in a child proof container (if a child take this can significantly reduce their bp and kill them)
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Nitroglycerin (SL) 0.4mg or 1/150 gr Take on q 5mins x 3 no relief call 911 Tablets will decompose when exposed to light and heat Keep in dark, glass, airtight jar. Not a child proof jar for decreased elder dexterity DO NOT SWALLOW UNDER GOES 1ST PASS METABOLISM AND WILL BE INEFFECTIVE
Transdermal is absorbed slowly.
You dont want to put the patches where you put the defibrillator because it will cause burns
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SL absorbed directly and rapidly into the internal jugular vein and right atrium. (40- 50% absorbed through GI are inactivated by liver metabolism)
Nitro-bid ointment (you dont want to get it on your hands because its a potent dialator and can pass out) and transdermal patch absorbed slowly through the skin Excreted primarily in the urine
Pharmacodynamics:
Causes the blood vessels of the blood vessels to relax and dialate
Decreases preload and after load, so the heart doesnt have to work as hard
Reduces myocardial oxygen demand
Onset action SL and IV: 1-3mins
Transdermal patches onset: 30-60 mins duration 24hrs
Sometimes pts can develop nitroglycerin tolerance. To help prevent this sometimes we would Remove patch for 8-12 hours to help pts not to become tolerance/ Remove patch 8-12hrs for nitrate free interval
Side effects: headache (very common; because of the potent dilation), hypotension, dizziness, weakness and faintness
Adverse reactions: taper dose to avoid REBOUND effect of severe pain due to myocardial ischemia, reflex tachycardia if given RAPIDLY.
Drug interactions: Remember, any medications that is going to lower bp, any other meds that also lower bp can cause a problem. Such as Betablockers, CA+ blockers, vasodialation and ETOH (alcohol) may cause hypotension
We want to make sure we are careful when we are utilizing these meds together
Nursing interventions of antianginals
-Monitor vital signs
*Check orthostatic hypotension (all antianginals lower blood pressure)
-offer a sip of water with the nitroglycerin; dont use fingers to apply ointment because it’ll cause a significant drop in blood pressure
- taper dose down; at risk of vasospasm and at risk of MI
Rotate patches, avoid dirty areas
Keep in storage containers
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Monitor vital signs Check orthostatic hypotension Offer sips of H2O prior to SL NTG to wet mouth and increase absorption DO NOT USE FINGERS TO APPLY OINTMENT DO NOT APPLY NITRI-BID OINMENT or Patch IN AREA OF DEFIBRILLATOR PAD PLACEMENT AS EXPLOSION OR SKIN BURNS MAY OCCUR Do not discontinue meds abruptly Rotate skin locations for patches and ointment, avoid hairy areas Keep in storage container
Cardiac dysrhythmias
Basically slows down the conduction within the heart.
We look at the ECG
When we have any interruptions in the p-wave, QRS, T, etc., thats when we see dysrhythmia
What are the common factors that causes dysrhythmias?
MI (after someone has had an MI, leads to dysrhythmias),
Hypoxia, hypercapnia,
Thyroid dx, CAD (blockages or plaques in the coronary vessels, leads to dysrhythmias), electrolytes imbalances (ex: potassium is conductor of the heart)
There are different types of antidysrhythmics
(Dont worry about what are the differences btwn the classes for example, the difference btwn class 1C and 1B)
Class I
Class II
Class III
Class IV
Class I
Class I are Sodium channel blockers
They decrease the sodium rush into the cells, which decreases conduction, which
**slows the heart and decreases ectopy
There are different types of class 1
What are the 3 types of Class I
Class IA
ClassIB
ClassIC
Class IA
A type of antidysrhythmic that Slows conduction and PROLONGS repolarization (PAT, SVT)
(Dont have to. Knoww these.. just to give you an idea what it is used for): PAT= paraschsmal atrial tachycardia …use it for atrial tachycardia/ rapid beating
SVT= regular rhythm, but beating over 150bpm
Meds: Quinidine, procainamide, disopyramide
Class IB
A type of antidysrhythmic that Slows conduction and SHORTENS repolarization (VT, fib)
Medications: lidocaine, mexitiletine HCL
(Extra info for better understanding: use for ventricular dysrhythmias /tachycardia)
Just focus on what rhythm each class is use for.
Class IC
A type of dysrhythmias that Prolonged conduction (VT, fib)
Medication: flecainide
Class II
A type of antidysrhythmic
These are your BETA BLOCKERS. Notice that they end in ‘olol’
Slows down the conduction speed (velocity) of the heart, help improve automaticity ; help decrease afibs, tachycardia, dysrhythmias
Meds: propranolol (Inderal),
acebutolol (Sectral), esmolol (Brevibloc),
sotalol (Betapace)
What is automaticity of the heart?
Automaticity is the property of cardiac cells to generate spontaneous action potentials
Acebutolol (Sectral)
Is a betablocker use for antidysrhythmias (keep in mind most beta-blockers are used for dysrhythmias)
Drug class: beta-1 blocker
Contraindications: anyone with heart block, severe bradycardia, severe HF, cariogenic shock
We know that taking a beta blocker will further decrease their hr and vasodilation
Interactions: anyone who is on meds that decrease their hr or bp ex: diuretics, prolonged hypoglycemia, antagonist effect with albuterol (albuterol causes tachycardia; have to look out for that), terbutaline, metaproterenol
Wat are the indications for acebutolol (Sectral)?
Treatment for dyshrythmias, angina, HTN
What are the side & adverse effects for acebutolol (Sectral)?
Dizziness, nausea, headache, hypotension, diaphoresis, fatigue
Remember if anyone on beta-blocker, have them taper down the dose.
Adverse: bradycardia, life threatening agranulocytosis (low WBCs) and bronchospasm at higher doses (remember, even in cardio selective meds, the lungs have a lil bit of beta-1)
Class III
At type of antidysrhythmics
Increase refractory period and prolong action potential
Indications: mostly used in atrial fibrillation (afib)
Amiodarone (Codarone)
Is a class III antiadysrhytmic
Increase refractory period and prolong action potential
Indications: mostly used in atrial fibrillation (afib)
Make sure to monitor thyroid function by doing tests, because thyroid may decline. It can also cause pulmonary fibrosis, so do pulmonary function tests.
Class IV
Class IV are calcium channel blockers
(Remember there are only two calcium channel blockers that lower hr; and use as antiadysrhythmcs )
Meds:
verapamil (Calan,Isoptin)
diltiazem (Cardizem)
They work by blocking calcium influx, which decreases the cardiac response and conduction
& put them back in normal sinus rhythm.
Contraindication: someone who has AV block, HF and severe bradycardia
(Dont want to decrease hr even more)
What are the drugs to help treat a Hyperlipidemia?
Bile acid sequestrants
HMG-CoA inhibitors
Fibrates
Niacin
Cholesterol absorption inhibitors
The goal is to put them on the highest tolerable dose without side effects, if we can’t do that we usually add these other medications
Bile Acid Sequestrants
To treat hyperlipidemia
They are usually added to statin (HMG-CoA inhibitors) to reach their goal cholesterol level
Indications: reduce elevated serum cholesterol in patients with hypercholesterolemia
Side/adverse effects of Bile acid sequestrants
Headache, fatigue, and drowsiness
Direct GI irritation: nausea and constipation
Increased bleeding times
Vitamin A and E deficiencies
What are the drug-to drug interactions with Bile Acid Sequestrants?
Malabsorption of fat-soluble vitamins
Thiazide diuretics, digoxin, warfarin, thyroid hormones and corticosteroids
HMG-coA Inhibitors
Aka ‘statin’ .. HCPs call them this
Utilize to lower cholesterol levels
Inhibits HMG-CoA, decrease serum cholesterol levels, LDLs, ad triglycerides and increase HDL levels
These are the best, best lowering
Indications: hyperlipidemia, prevention MI, CVA
Medications: atorvastatin (Lipitor),
rosuvastatin (Crestor),
Simvastatin (Zocor),
Lovastatin (Mevacor),
Pravastatin (Pravachol)
notice that they all end in ‘statin’
Where is the HMG-CoA inhibitor mainly metabolized?
Through the main pathway in the liver ,
So if someone is an alcoholic, liver toxicity, taking other meds that are metabolize through that,..typically try not to use that statin.
What are the contraindications of HMG-CoA inhibitors?
Allergy, active liver disease and hxs of alcoholic liver disease, pregancy and lactation
Caution in impaired endocrine function because they can develop hyperglycemia.
Why pregnant women or women, who are lactating cannot take HMG-CoA Inhibitors/statin?
Because babies need fat and cholesterol to have normal brain development, so we should never never ever put a woman who is pregnant or breast feeding on any cholesterol lowering medications.
What are the adverse effects of HMG-CoA?
Myopathy (complain in muscle pain)
Liver failure
Rhabdomyolysis (break down of all the muscle tissue and lead to organ failure; deadly)
Do liver function tests to monitor
Drug-to-drug interactions with HMG-CoA inhibitors
Erythromycin
Cyclosporine
Gemfibrozil
*Niacin
Grapefruit juice (also metabolize in the same pathway)
Acetaminophen:
It takes the same pathway as the satin, so pt should limit use of taking acetaminophen
Rosuvastatin (Crestor)
Class: A HMG-CoA inhibitor
Which decreases lipid levels (especially LDL and triglycerides)
Commonly use
Side effects: HA, constipation, diahreah, myalgia (muscle pain)
Adverse reactions: rhabdomyolysis (break down of muscle tissue; lead to death), photosensitivity, hyperglycemia, elevated LFTs
Contraindicated: pregnant, lactation, liver dx
Caution with ETOH use, Tylenol use, hxs of liver disease
Monitor LFTs at 6-8wks, then 6 months and then yearly
Cholesterol Absorption Inhibitors
Used to treat hyperlipidemia
Work in the small intestines to inhibit the absorb of cholesterol
This is typically an additive treatment, (for example, if someone cant get to their LDL goal on a highest tolerated dose of statin or they cant tolerate statin, we put them on cholesterol absorption inhibitor)
Med: Zetia (ezetimbe)
What are the indications of cholesterol absorption inhibitors?
To lower serum cholesterol levels,
Treat homozygous familia hypercholesterolemia
What are the pharmacokinetics of cholesterol absorption inhibitors?
Absorbed in the GI tract,metabolized in the liver, excreted in urine and feces
Adverse/Side effects of cholesterol absorption inhibitors?
Abdominal pain and diarrhea
Headache
Dizziness
Fatigue
URI (upper respiratory infection)
Back pain
Muscle aches and pain
What are the drug-to-drug interactions of cholesterol absorption inhibitor?
Not significant but soemthing to keep in mind
Cholestyramine
Fenofibrate
Gemfibrozil
Antacids
Cyclosporine
Vibrates
Warfarin
Wha are the contraindications of cholesterol absorption inhibitors?
Allergy
And remebr pts who are pregnant or breast feeding if combined with a statin.
Niacin
Another lipid lowering agent
Vitamin B3, inhibits release of free fatty acids from adipose tissue.
Increase rate of triglyceride removal from plasma.
With this, they sometimes develop redness in chest or head; NOT an allergic reaction; its a known reaction
Fenofibrates
Used to treat hyperlipidemia
An additive to statin
Inhibits triglyceride synthesis in the liver, which decreases LDL
Increase Uric acid secretion and may stimulate triglyceride breakdown
Gemfibrozil
Another lipid lowering agent
Inhibits peripheral breakdown of lipids
Reduces production of triglycerides and LDL
Increases HDL
If combine with statin, we need to watch the LFT because both goes through same metabolic pathway.
Think of the gem’FIBR’ozil in FenoFIBRates
PSK9 Inhibitors
Help reduce LDLs and triglycerides
Not metabolized by the liver, and does not cause muscle aches and pains
Meds:
alirocumab (Praluent)
Evolocumab (repatha)
“PSK9 Ihibits CUM”
Injectable lipid lowering therapy (PSK9 Inhibitors) are only used when
When patients CANNOT tolerate statins
Or
Pts not at a goal at highest tolerable statin dose (ex: still had muscle aches and pains)
Or
They have liver toxicity and cannot be put on a statin
Can also use as a Addive
Patient education of PSK9 Inhibitor
Kept in the refrigerator take out fridge 30mins before taking dose
Make sure to hold down pen until windows fills with yellow tube.
Peripheral Vasodilators
Class: peripheral vasodilator
For those who have peripheral vascular disease.
Dilates those lil arteries in the extremities to improve blood flow to the tissue.
Indications: pts who have clottictaion/ angina in the legs
/
Increase blood flow to the extremities in older adults with PAD and PVD
Also effective in Raynaud’s disease, and Buergers disease
Meds:
cilostanzol (Pletal)
Trental
(Think of petals from roses look like platelets 🌹…”tal” ending in peripheral vasodilators)
Pletal
Class: peripheral vasodilator
Trade name: cilostazol
Therapeutic effects: Prevent platelets from sticking together/ Inhibits platelet aggregation and causes vasodialation
Use for peripheral vascular disease; it increases circulation.
Treats Raynaud’s disease, and cerebral vascular insufficiency.
PO
Interactions: hypotension, with anti-hypertensives
Never use Pletal for ___?
For patients who have. Stents
Contraindications in Pletal
Pts that have heart failure, arterial bleeding (you’re increasing secretions/ increase blood loss), severe hypotension, postpartum, tachycardia
Caution: bleeding disorder & tachycardia.
Side/adverse effects of Pletal
N/V
Dizziness
Syncope(fainting)
Blood in the eye
HA
Abdominal pain
Abnormal stools
Peripheral edema
Adverse: tachycardia, palpitations
Nursing considerations for Pletal
Obtain baseline vitals
Asses their extremities and observe for signs of inadequate blood flow to the extremities: pallor, coldness, and pain …see any improvement
Monitor for tachycardia & hypotension.
Thrombosis
Formation of a clot
What are the different types of blood clots?
Arterial (WBC & RBC)
Blood stasis (the blood is not moving; form clots ; thats why we have compression stockings on)
Platelet aggregation (if there’s plaque on the arteries; platelets can build up and form a clot)
Blood coagulation
Venous (RBC and PLT) happens in the veins
Blood stasis of slow flow
Occur rapidly
Can cause DVT and can lead to a Pulmonary embolism
Anticoagulants
Help prevent blood clots form forming
Ex: if someone is just sitting around, and the blood is just sitting there, it will help the blood clot from forming.
If someone already HAS a blood clot, it will prevent the clot form getting bigger. (It does not break up the clots; thrombolytics does) Alow THE BODY to break down the clot.
Indications for anticoagulants
Pts with both arterial and venous clots or pts who are at risk for clot formation
DVT
Pulmonary embolisms
MI (can be caused by blood clots
Artificial valves(the body doesnt recognize that surgery is good; the body see it as an injury; increase risk of forming clots; thats why its ideal to give Heparin during surgery)
CVA (stroke;
What are the different types of anticoagulant medications?
Heparin
Lovenox (LMWH)
Coumadin (LMWH)
Fragmin(LMWH)
Innohep (LMWH)
Heparin
used for RAPID anticoagulation for thrombosis such as DVT, PE, CVA (cerebral vascular accident)
Mostly used via IV
Used during surgery it is given to prevent thrombosis.
We use it as a bridge (ex: if someone is using another agent such as Coumadin and coming into a hospital for a procedure, we would take them off and then put them on heparin)
What is the mode of action of Heparin?
Combines with antithrombin III and *prevents thrombin formation
Inhibits the conversion of fibrinogen to fibrin *prevents fibrin clot formation
Prolongs clotting time Partial thromboplastin time (PTT)
How you measure heparin?
By looking at the PTT (partial thromboplastin time)
Ex: if the levels are too high, i need to lower dose of heparin)
Why Heparin is not given in other routes, besides IV and SQ?
Because heparin is poorly absorb through the GI mucosa
It is destroyed by heparinase in the Liver
Poor oral absorption
Not given IM due to pain and hematoma formation
How do you administer Enoxaparin (Lovenox)
2 inches away from umbilical
Maintain air bubble
What are the side/adverse effects of Heparin?
Bruising
Itching
Burning
Adverse Effects:
Beeding
Ecchymosis (bleeding under skin )
Thrombocytopenia (having an allergy to heparin; HIT: heparin induce thrombocytopenia)Increase risk of blood. Clot
Hemorrhage (can be life-threatening)
What are the contraindications of heparin?
Bleeding disorder
Peptic ulcer (increase risk of GI bleed)
Severe hepatic or Renal disease
Hemophilia
Hemorrhagic CVA/stroke: means they are already bleeding;it’ll increase tremendously with heparin)
What are the drug and food interactions of Heparin?
Taking another drug that is also an anticoagulant, there is going to be a higher increase of bleeding.
Increase effect with ASA (aspirin), NSAIDS, thrombolytics and probenecid
Decresed effect of nitroglycerin and protamine (antidote)
If someone is hemorrhaging from heparin, and we want to reverse it, what antidote do we use?
Protamine
Nursing consideration with heparin
Obtain hxs of possible abnormal clotting or health problems affect clotting (i.e. ETOH, severe renal or liver disease)
PTT should be checked (usually we start them on heparin and check the PTT 4 hours later or anytime we change the dose check 4 hours later)
Check stool for melena (dark starry blood stool) and occult blood (do a guiac) to see if there is any GI bleed
Warfin (Coumadin)
An anticoagulant
Same indications as heparin
Only given PO
Inhibits vitamin K, which decreases the clotting of blood
Its given at home
We need to worry about what they are eating; vitamin K will counter interact with Warfin.
Warfin (Coumadin) is affected by high type of foods?
Foods with vitamin K: dark leafy greens
Decreases the effectiveness of Coumadin and lower INR
Pts on Coumadin, they need to eat the same amount of dark green veggies every week (ex: if they normally eat it 3xs a week, you can do so and be consistent ) & adjust the Coumadin based on how much dark green leafy veggies they eat and according to their Pt/INR
If someone has HIGH INR, the antidote is vitamin K
Antibiotics often increase INR; monitor closely
What happens when the INR is high?
Pt is at increase risk of bleeding
We also look at their INR to adjust what?
To adjust the Coumadin dose.
If INR is too low, and they are at risk for blood clots, will need to increase the dose of Coumadin
If their INR is too high an increase of bleeding; would lower the dose of Coumadin.
Therapeutic range for INRS
Therapeutic range means that the Coumadin is preventing the blood form clotting
Normal INR range (someone who is not taking Coumadin): <1.2
*AFIB (therapeutic range): 2-3
*DVT/PE (therapeutic range): 2.5-3.5
High INR
MEANS INCREASE RISK OF BLEEDING
LOW INR
INCREASE RISK OF CLOTTING
Therapeutic INR
What the disease process is and what we know that will prevent blood clots from working
Novel anticoagulants
Aka NOax
New to the market
No INR monitor (no blood tests)
No antidotes yet
Increased risk for bleeding but less than warfarin
Most dose adjusted for renal insufficiency
Utilize for pt that have atrial fibrillation, DVT /PE BUT NOT USED FOR PTS THAT HAVE a MECHANICAL VALVE
Oral
Medications:
Eliquis (apixaban),
Xarelto (rivaroxaban),
Pradaxa (dabigatran)
“Novel AN!”
Dabigatran etexilate (Pradaxa)
A NOax aka Novel anticoagulant
Think of “NO’axa’”
These help prevent blood clots from forming
Treatment for DVT/PE and prophylaxis, stroke prophylaxis (non-valvular atrial fibrillation)
We need to worry about if they have chronic kidney disease; have to adjust dose; because it is mostly excreted by the kidneys
Avoid in hemodialysis
What are the side/adverse effects of Dabigatran etexilate (Pradaxa) ?
Side effects: bleeding, bruising, gastritis
Adverse effects: hemorrhage, hematoma, thrombocytopenia
What is the black box warning for Dabigatran (pradaxa)?
If pts are taking off this medication they have an increase risk of a blood clot forming
If they are on this medication, they cannnot get epidural because it will cause a spinal hematoma risk
What is the antidote for Dabigatran etexilate (paradaxa)?
Praxibind
Apixaban (Eliquis)
&
Rivaroxaban (Xarelto)
Class: Novel Anticoagulants
Therapeutic use: thromboembolism (DVT/PE) treatment and prophylaxis, stroke prophylaxis (non-valvular artrial fibrillation)
It blocks one of the clotting factors “Xa”
Excreted by kidneys;; decrease dose in CKD; avoid hemodialysis
Side effects: bleeding, bruising, gastritis, anemia
Adverse effects: hemorrhaging, hematoma, thrombocytopenia
Black Box Warning: increase thrombotic event and stroke risk when discontinued prematurely, epidural and spinal hematoma risk
What is the black box warning for all novel anticoagulants?
Increase risk to form a blood clot and pt cant get epidural it is a hematoma risk
Antiplatelets
Are a lil different
Help to prevent platelets from sticking together or aggregating together
Indications: use for pts who have MI or CVA(blockage in coronary arteries) , Stroke (not hemological stroke)
What are examples of antiplatelet medications?
ASA (aspirin),
*Ticagrelor (Brilinta) must use with 100mg ASA or less (usually 81)
Effient (prasugrel)
Clopidogrel (Plavix)
*Pletal (remeber use it for peripheral vascular disease NOT CVA)
Agrylin
Reopro
Integrillin
What do you need to remember with Ticagrelor (brilinta)?
Its an antiplate
It doesnt work if a person is on aspirin for more than 100 mg a day .
The aspirin has to be less than 100mg. (Or just 81mg)
Clopidogrel (Plavix)
Class: Antiplatelet
Helps to prevent blood clots from sticking together
Indication: prevent recurrence of MI or stroke, and prevent vascular death
In order for Clopidogrel (Plavix) to work, what type of dose they need to be placed on?
Need to start off with loading dose in order for it to work. Its either 300 or 600 mg they would have to take all at once.. then taken 75mg everyday
Contraindication of Clopidogrel (Plavix)
We do not use it in someone who is bleeding (intracranial bleed or hemorrhage)
Peptic ulcer
you do NOT keep them on an antiplatlet medication if the had BRAIN or SPINAL surgery
Caution: anyone who is undergoing surgery going to be careful with;
Liver disease
GI bleeding
Bleeding from trauma
Side/Adverse effects of Clopidogrel (Plavix)
Side:
URI (upper respiratory infection)
Flulike symptoms
Dizziness, HA , fatigue, CP (cerebral palsy), diahrea,
*Bleeding, *bruising
Adverse reactions: HTN, bronchitis
WHat are the interactions with Clopidogrel (Plavix)
May increase bleeding with NSAIDs (like ibuprofen, Motrin; any anticoagulants)
Interferes the metabolism of:
Warfin
Phenytoin
Fluvastatin
Tamoxifen
Tolbutamide
Torsemide
Ginger, garlic, ginkgo, feverfew increase risk of bleeding
Remember meds that are anticoagulants increase risk of bleeding
What are the difference btwn Antiplatlets and Anticoagulants?
Anticouagulatnts prevent BLOOD CLOTS from forming they are only utilize for pts who has ATRIALFIBILLATION, DVTs or PEs
Antiplatlets medications prevent PATLETS from sticking together and use for pts who have HEART DISEASE or hxs of STROKE or PERIPHERAL VASCULAR DISEASE
Summary:
Anticoagulants, such as heparin or warfarin (also called Coumadin), slow down your body’s process of making clots. Antiplatelets, such as aspirin and clopidogrel, prevent blood cells called platelets from clumping together to form a clot
In general,
-Anticoagulants are used for conditions that involve stasis. Stasis can cause blot clots (thrombosis) to form. That’s why PCDs are used for DVT prophylaxis.
-Antiplatelets are used for conditions that involve endothelial damage and platelets sticking to the injured site. For example, in the heart, ischemia and MI are usually not due to stasis but to plaque formation with coronary vessels. So you use antiplatelets.
Thrombolytics
“These are clot busters”
Used to promote the fibrinOLYYTIC mechanism /ACTUCALLY BREAK UP THE CLOT
indications: Utilize it pts who are having a STROKE (remember, we have to make sure it’s a embolic stroke and not a hemorrhagic stroke),
MASSIVE MI
MASSIVE PE
MASSIVE DVT
CVA (embolic stroke only; not hemorrhagic)
Having an acute MI Breaks up the clot and and open up the arteries
Or
If someone has a very big PE, use a thrombolytic to break up the clot
The most potent and powerful; so the. HIGHEST risk of bleeding is with these medications
When does the thrombolytic starts to work or the onset of it?
Usually the thrombus or clot disintegrates Within 4hours of the disease process
What are the types of thrombolytics?
Streptokinase,
Urokinase,
Altepase
Reteplase (retevase)
Tenecteplase (THKnase)
“ pASE give me a thrombolytic!!!!)
Ateplase (tPA)
Class: Trhombolytic argent
It breaks up the clot
To help improve blood flow
Indications: dissolve clot following AMI (acute myocardial infraction), PE, acute ischemic stroke
Side effects: bleeding
Adverse: biggest risk is intracranial bleeding, stroke, atrial or ventricular dysrhythmias
This medication is short term
What are the contraindications of Ateplase (tPA)
Internal bleeding,
bleeding disorders,
recent CVA/Stroke (even if is is an embolic stroke, a lot of times it can lead to a hemmoragic/bleeding stroke)
Surgery or Trauma
Bacterial endocarditis
Sever liver dysfunction
Severe uncontrolled HTN
Drug-food interaction with Ateplase (tPA)
Increase bleeding when taken with oral anticoagulants, NSAIDS, cefotetan, pilcamycin
Sodium-Glucose Co-transporter 2
(SGLT-2) Inhibitors
Aka “SOG2”
Class: Antidiabetic medication
Decrease blood glucose levels; cause body to get rid of glucose through urine. Have to be careful because can increase fungal infections and UTIs
Use in pts who has HF and protect the heart from getting damaged,, while getting rid of glucose (especially those who has HF and diabetes)
Dont use it to treat type 1 diabetes; insulin would be the one to use for that
Medications:
Empagliflozin (Jardiance),
Canagliflozin (Invokana),
Dapagliflozin (Farxiga)
Ending in “gliflozin”
WHat are the things to worry about with pts on Sodium-Glucose co-transporter 2 Inhibitors?
A/E: Hyperkalemia, fungal infections, UTI, renal insufficiency and
could potentially develop Hypotension (because when the glucose is leaving the body by urine, sometimes increasing urine production, and cause pt to become dehydrated; leads to hypotension)
Sacubitril/Valsartan (Entresto)
“Sartan” is an ARB
Also used for pts who have HF, help to reduce the morbidity and mortality of HF
Indications: heart failure with reduced ejection fraction
Side effects: hypotension, dizziness, cough, Hyperkalemia, real failure
Adverse effects: hypersensitivity, angio edema, severe hypotension, renal failure
Black box warning: fetal toxicity
What are the drugs to treat COPD
Bronchodialators (sympathomimetics, Beta-2 adrenergic agonist)
Methylxanthines (xathines)
Leukotriene antagonists
Glucocorticoids
Cromolyn
Anticholinergics
Mucolytics
Beta2 adrenergic agonists
It is a sympathomimetic
Alpha and beta2 adrenergic agonists
They STOP the bronchoconstriction and help to relieve Sxs of asthma or COPD exacerbation
Examples:
albuterol (Proventil), Ventolin, Metaproterenol
Albuterol (Proventil)
Class: Beta-2 Adrenergic
Indication: used for acute asthma attack, control asthma, exercise induced asthma (when exercise triggers their asthma)
Rapid onset; thats why we can use it as a rescue medication
What do we worry about with albuterol (Proventil) medication?
Can potentially affect Beta 1 as well.. remember the heart has a bit of beta-2.. thats why they can have heart palpitations, tachycardia hen on this medication
What is an alternative for pts who have afib or tachycardia who is experiencing an asthma attack?
Xopenex
Less heart rate, and good for pts with afib or tachycardia
How to use an Aerosol inhaler? (MDI (meter dose inhaler) or DPI (dry powder inhaler)
Always test spray inhaler that hasn’t been used recently
Insert medication canister into plastic mouthpiece
Shake inhaler before using, remove cap from mouthpiece
Breath out through mouth, place mouthpiece 1-2 inches from mouth or in mouth
Take slow deep breath while pressing top of medication canister once
Hold breath for few secs, exhale slowly through pursed lips
Wait two minutes repeat starting from shaking again
Administer bronchodilator 1st, wait 5mins then steroid inhaler (the steroid can actually get into the lungs)
Ipratropium (Spiriva)
Class: Anticholinergic
Indications: for maintance treatment of bronchospasm associate with COPD
To relax the bronchotubes and prevent bronchoconstriction
Administer this before administering the steroid, because we want to dilate the airway, so the steroid can get in.
How long to administer steroid after administering the Spiriva?
Administer Spiriva 5 minutes before steroid or cromolyn (this allows the bronchioles to
dilate so the steroids or cromolyn can be deposited in the bronchioles
What are the side/adverse effects of Spiriva?
Side effects: dry mouth, hoarseness
Adverse effects: angioedema (allergic reaction), dehydration, hyperglycemia
What are the Contraindications of Spiriva?
Cannot use during pregnancy
If someone is allergic to peanuts or lactose
Glaucoma (remember increasing ocular pressure)
Breastfeeding
Methylxanthine (xanthine) derivatives
Used for treatment of asthma
Stimulated the CNS (think of sedative effect) and respiration
Examples are aminophylline, theophylline and caffeine
They all have “ine” endings
*Therapeutic range: 10-20 mcg/ml ; the higher above that 20, the more side effects they have