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

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/133

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

133 Cards in this Set

  • Front
  • Back
nitroglycerin - actions
decreases oxygen demand on heart

dialates arteries and veins

reduces blood volume

decreases preload on heart
nitroglycerin - uses
angina pectoris
nitroglycerin - common adverse effect
excessive hypotension
prolonged
headache
tolerance
nitroglycerin - indication
most common drug to treat angina pectoris (drug of choice)
nitrate - medication administration forms
sublingual tablets

substance release - capsules, tablets, ointment, transmucosal tablets, transdermal patches

translingual spray

amyl nitrite for inhalation (glass vials)
nitrates - sublingual tablets
Disolves rapidly. Primary for acute attacks
Nitrates - substance release - capsules, tablets, ointment, transmucosal tablets, transdermal patches
used prophylactically to prevent angina attack
Nitrates - translingual spray
used prophylactically and acute to prevent angina attack
Nitrates - amyl nitrite for inhalation
glass vials
chronic stable angina
Precipitated (caused) by stress or exertion

Short duration

Relieved by rest or nitroglycerin

Probable cause: fixed atherosclerotic obstruction (fix the plaque = fix the pain)
Unstable Angina
Unpredictable; changes in frequency, duration, and onset

Probable cause: atherosclerosis and thrombus formation
Variant Angina
Occurs at rest,

characteristic ECG changes

Probable cause: vasospasm of the coronary artery
Angina Pectoris
Chest discomfort arising from the heart due to lack of oxygen to the heart muscle
Angina pectoris - signs and symptoms
Squeezing in the chest, pressure, tightness, choking, burning, heaviness, may radiate to neck, shoulder, jaw
Angina Pectoris - Causes (precipitating factors)
Physical activity, exposure to cold, drinking caffeine-containing beverages, smoking, emotional stress, sexual intercourse, eating large meals
Angina Pectoris Treatment - Goals
Prevent myocardial infarction and death
Pain relief
Angina Pectoris Treatment - treatment
drug therapy - nitrates/beta blockers

step 1 - Coronary angioplasty - they place a stent (hollow metal tube) where the blockage occurred.

Step 2 - Coronary artery bypass surgery - they take a good vessel from a leg and replace it with the bad coronary vessel
Angina Pectoris - Patient education
Avoid precipitating factors (cause)
Reduce risk factors
Exercise
Angina attack duration
30 seconds to 30 minutes
Drugs to treat Angina Pectoris
Nitrates
Beta-adrenergic blocking agents
ACE inhibitors
Calcium channel blockers
Fatty oxidase enzyme inhibitors
Statins
Platelet-active agents
Angina pectoris - treatment
Morphine - pain and vasodialating effects
Oxygen - reduces workload of the heart
Nitro - vasodialator
Aspirin - antiplatelet/reduces/prevents blood clots
Angina Pectoris - Patient education
Correct use of prescription medications
Common adverse effects from prescription medication
Avoid fatigue and cold weather
Lifestyle modifications
Smoking cessation referral, if necessary
Always stop activity or exercise when chest pain is present
Nitro-BID
topical ointment

onset 30 minutes

duration 3 hours
Nitro-Dur
Patch, Transmucosal

onset 30-60 minutes

Duration - less than 24 hours
Nitrolingual
Spray, translingual

onset 2 minutes

Duration 30-60 min
Nitroglycerin IV
IV Fluid

onset 1-2 minutes

Duration 3-5 minutes
NitroStat
Tablet sublingual

Onset 1-2 minutes

duration less than 30 minutes
Beta blockers - Use
Reduce the number of anginal attacks
Reduce nitroglycerin use (patient will use less nitro if on beta blockers)
Anti-hypertensive (reduces blood pressure)
Beta blockers - actions
Block beta adrenergic receptors in heart (reverses sympathetic nervous responses)
Reduce myocardial oxygen demand
Reduce blood pressure (reduces hypertension)
slows heart rate down
slows cardiac output
inhibits renin release = prevents vasoconstriction
digoxin antagonsist
Digibind (Digoxin Immune Fab)
Narcotic antagonist
Narcan (naloxone)
Benzodiazapine antagonist
Romazicon (Flumazenil)
Heparin Antagonist
Protamine
Coumadin antagonist
Vitamin K (Phytonadione)
Tylenol antagonist
Mucomyst ( Acetylcysteine)
Diuretics - uses
Used to increase flow of urine to reduce excess water in the body

Primarily used to treat heart failure, hypertension

Other uses:
liver disease,(spironolactone)

renal disease,(Lasix)

cerebral edema & increased intraocular pressure (mannitol)

treat hypercalcemia (lasix)
Diuretics - therapeutic outcomes
reduce edema

improve symptoms of excess fluid
Pathologic Conditions Contributing to Excess Fluid
Heart failure - leads to:

Edema, adventitious (abnormal) lung sounds, dyspnea, change in mental status

Liver disease - leads to:

Jaundice (yellow skin) , ascites (edema of the stomach area) , disorientation, history of alcohol dependence, overdose of OTC medications
Adverse outcomes if diuretics not given
renal failure (kidney)
pulmonary congestion (water in the lungs)
edema
hypertension
stroke
death
Renal Function Assessement
History of related causative disorders/factors

History of current symptoms

Pattern of urination - frequency nocturia

Medication history

Hydration status

Electrolyte imbalance (low/high na or K)

Often subtle changes, such as in mental status, muscle strength/cramps, tremors, nausea, general appearance
Nursing assessment for hydration status - (ways to know diuretics are working)
Evaluate for dehydration: skin turgor, oral mucous membranes

Monitor laboratory values for changes

Evaluate location of edema, signs of reduction

Obtain daily weights- 1 liter= 1kg

Measure intake and output

Orthostatic Vital signs
Diuretics - Electrolyte Imbalance
Susceptible people: history of renal or cardiac disease, hormonal disorders, massive trauma or burns

Assess mental status, muscle strength and cramps, tremors, nausea, general appearance


Serum potassium < 3.5 mEq/L (hypokalemia), > 5.5 mEq/L (hyperkalemia)

Serum sodium < 135 mEq/L (hyponatremia), > 145 mEq/L (hypernatremia)
Patient education - diurectics
Accurate measurement of fluid intake and output

Purpose of diuresis (HTN, glaucoma, CHF, Renal disease)

Medication considerations (take in AM)

Nutrition- Na+ sodium , K+ potassium alert (avoid or increase high K/NA foods) depending on type of diuretic taken (potassium sparing or not).

Potassium sparing diuretics can cause hyperkalemia.

Health maintenance

Written record/patient self-assessment form- extremely important for pt to track. At least in the begin of therapy.
Carbonic Anhydrase Inhibitor - Actions
Weak diuretic; inhibits the enzyme carbonic anhydrase in kidney, brain, eye
Carbonic Anhydrase Inhibitor - Uses
Reduces intraocular pressure with glaucoma (high eye blood pressure- glaucoma can cause blindness)

reduce seizure activity with certain types of epilepsy

Not used frequently, but effective for decreasing IOP.
Carbonic Anhydrase Inhibitor - drug
Acetazolamide (Diamox)
Sulfonamide-Type Loop Diuretics - Drugs
Bemetanide (Bumex),Furosemide(Lasix)
Sulfonamide-Type Loop Diuretics - Actions
Actions
Inhibit sodium and chloride reabsorption in ascending limb of the loop of Henle
Sulfonamide-Type Loop Diuretics - uses
Uses
Treat conditions such as edema resulting from heart failure, cirrhosis of the liver, renal disease (proteinuria)
Sulfonamide-Type Loop Diuretics - Adverse effects
Common adverse effects

Oral irritation, dry mouth; orthostatic hypotension

Serious adverse effects

Abdominal pain; electrolyte imbalance, dehydration; hyperuricemia (too much uric acid in your blood) hyperglycemia; hives, pruritus (r/t sulfa)
Thiazide Diuretics - drugs
HCTZ all end in (azides)
Thiazide Diuretics - actions
Block reabsorption of sodium and chloride ions from the distal tubule

less effective over time - due to tolerance
Thiazide Diuretics - Uses
Uses
Treat edema associated with heart failure, renal disease, hepatic disease, pregnancy, obesity, premenstrual syndrome
Thiazide Diuretics - Adverse effects
Common adverse effects
Orthostatic hypotension (mild)

Serious adverse effects
Electrolyte imbalance, hyperuricemia, hyperglycemia
Potassium-Sparing Diuretics - drugs
Drugs: amiloride (Midamor), spironolactone (Aldactone), triamterene (Dyrenium)
Potassium-Sparing Diuretics - actions
Induce retention of potassium; excrete sodium at the distal renal tubules. Weak anti-hypertensive activity.
Potassium-Sparing Diuretics - uses
In combination with other diuretics to treat edema,hypertension or heart failure, prevent hypokalemia
Potassium-Sparing Diuretics - Adverse effects
Common and serious adverse effects: N/V, anorexia,headache,electrolyte imbalance, dehydration.
Potassium values
Serum potassium less than < 3.5 mEq/L = hypokalemia

Potassium greater > 5.5 mEq/L = hyperkalemia
Sodium Values
Serum sodium less than < 135 mEq/L = hyponatremia

Sodium greater than > 145 mEq/L = hypernatremia
Drugs that affect potassium
Beta blockers - increase potassium
Ace inhibitors - increase potassium

Diuretics - decrease potassium except for potassium sparing diuretics.
diuretic that work on loop of henle
furosemide - lasix
bumetanide - bumex
toresemide - demadex
ethacrynic acid - edecrin
diuretics that work on distal convolution
spironolactone
triamterene
amiloride
Thiazides
diuretics that work on the proximal convolution
osmotic diuretics
Thrombolitic disease
the process of forming a blood clot or thrombus

Fragments of a thrombus can break off and circulate until trapped in a capillary, creating an embolus

Clotting cascade is activated when a blood vessel is injured, or with increased viscosity
Intrinsic clotting pathway
Is initiated by the blood coming in contact with exposed collagen in the blood vessel wall, i.e., material within the blood or blood vessel wall.
Extrinsic clotting pathway
Is initiated with material outside of or "extrinsic" to the blood.
Conditions that cause clots to form (Risk factors)
Immobilization with venous stasis
Surgery, trauma to lower limbs
Heart failure, vasospasm
Cancers of the lung, prostate, stomach, pancreas
Pregnancy, oral contraceptives
Diabetes
Truck Drivers
Bed Ridden
Stasis prevention
leg exercises
wearing stockings
leg elevation
sequential compression devices - device that includes a wrap on your legs and is connected to a pump that squeezes so blood circulates back to the heart.
Revascularization treatments
(treatments that reroute blood flow through vessels)

percutaneous coronary intervention - stent (metal tube creating opening of clogged vessel)

coronary artery bypass graft - take a vessel from elswhere in the body and graft it on the coronary artery
Drug Therapy Goals for Thromboembolic Diseases
Primary purpose is to prevent platelet aggregation or inhibit steps in the clotting cascade
4 types of thrombolitic treatments
Platelet inhibitors
Anticoagulants
Glycoprotein IIb/IIIa inhibitors
Thrombolytics
Anticoagulation therapy treatment
Prevents new clot formation

Treats existing clots
Thrombus interventions
Do not massage area that may have a clot. Clot can dislodge and go to brain or lungs

evaluate pulse color temperature of skin
Coagulation tests (blood test)
PT (prothrombin time) - pt value will determine adjustment of coumadin.

aPTT (activated partial thromboplastin time) - aPTT value will determine the adjustment of Heparin.

INR (international normalized ratio)
Platelet counts
PT (protrombin time) lab value
determine increase or decrease adjustment of coumadin medication
aPTT (activated partial thromboplastin time) lab value
Determines the increase or decrease adjustment of Heparin.
Aspirin - uses
antiplatelet therapy

reduces frequency of:

TIA - transient ischemic attack - temporary stroke due to temporary lack of blood to the brain.

Ischemia= lack of blood flow

Reduces frequency of MI - Myocardio Infarction
Aspirin - Actions
Inhibits platelet aggregation for the life of the platelet (stops clumping)

Prolongs bleeding time
MI - Myocardio Infarction
heart attack
Plavix - uses
reduce risk of ADDITIONAL: (for people who already have had the following)

myocardial infarctions (MI)
Strokes
Vascular death (vessel death)

may be used together with aspirin
Plavix - actions
Inhibits/disrupts the ADP pathway (aggregation process) required for platelet aggregation

Prolongs bleeding time - person will bleed longer

prolonged bleeding time is beneficial for patients with weak hearts so that the blood will not thicken due to weak contractions of the heart. Same applies to Aspirin
lovenox (eoxaparin) - actions
Low molecular weight heparin (LMWH)
Less potential for hemorrhage
longer duration of action
Prevents coagulation cascade
no antiplatelet activity
does not affect PT or aPTT
Lovenox - uses
prevent DVT (deep vein thrombosus) after hip, knee or abdominal surgery

Treat DVT along with coumadin

Treatment of STEMI (ST elevation MI)

Derived from pigs - should not be given to patients allergic to pork
Heparin - action
natural substance extracted from gut of pigs and cows

inhibits clotting factors

No fibrinolytic qualities (cannot bust a clot)
Heparin - Uses
treats
DVT
Pulmonoary embolisms
peripheral arterial embolisms
MI
hemodialysis (filtering of blood by machine outside the body)
PCI - percutaneous coronary interventions (stent placement)
Heparin - administration points to remember
never give po
do not aspirate this drug
can be given subq or IV
Platelet inhibitors - common adverse effects
Abdominal distress
hypotension
Platelet inhibitors - serious adverse effects
Serious adverse effects
Neutropenia
agranulocytosis - low white blood cells
bleeding
Anticoagulant - patient education
Diet and nutrition
Limit intake of leafy green vegetables
Drink six to eight 8-ounce glasses of fluid daily
Exercise and activity after surgery to prevent venous stasis
Do not flex knees or place pressure under knees; avoid being motionless
Medication regimen
Dose and timing, common and serious adverse effects, drug interactions
Anticoagulants - adverse effects
Common adverse effects

Hematoma formation (blood collection under the skin)

bleeding at injection site

Serious adverse effects

Bleeding
thrombocytopenia (low blood platelets)
Anticoagulants - assessment for bleeding
Monitor to detect hemorrhage
Symptoms of internal bleeding
Decreased blood pressure, increased pulse, cold clammy skin, faintness, disorientation
Consider all areas of the body that could begin to bleed (visible and internal)
Monitor laboratory values
aPPT, platelets, hematocrit
Drug Class: Glycoprotein IIb/IIIa Inhibitors - drugs
Drugs: abciximab (ReoPro), eptifibatide (Integrilin), tirofiban (Aggrastat)
Drug Class: Glycoprotein IIb/IIIa Inhibitors - Actions
Actions
Block receptors on platelets, preventing aggregation and clot formation
Drug Class: Glycoprotein IIb/IIIa Inhibitors - Uses
Uses
Prevent clots forming from the debris often released during percutaneous coronary intervention (PCI) procedures
Drug Class: Glycoprotein IIb/IIIa Inhibitors - Serious side effects
Serious adverse effects
Bleeding
thrombocytopenia
Fibrinolytic Agents - uses
Uses

Dissolve fibrin clots secondary to coronary artery occlusion (MI), pulmonary emboli, cerebral emboli, deep venous thrombosis
Fibrinolytic Agents - actions
Actions
Stimulate the bodies own clot-dissolving mechanism, converting plasminogen to plasmin, which digests fibrin
Fibrinolytic Agents - drugs
Drugs: streptokinase, alteplase (Activase), reteplase (Retavase), tenecteplase (TNKase)
Fibrinolytic - contraindications
active internal bleeding recent (within 2 months)

cerebrovascular accident

intracranial or intraspinal surgery

severe uncontrolled hypertension

pregnancy
Heart Failure - Definition
Cluster of signs/symptoms that arise when the ventricles (left, right, or both) lose ability to pump enough blood to meet the body’s circulatory needs
Systolic dysfunction (contraction dysfunction)
Heart Failure - Symptoms
decreased exercise tolerance
poor peripheral tissue perfusion
Diastolic dysfunction (filling dysfunction)
pulmonary congestion
pulmonary edema
Heart Failure - how it works
Body Compenates by:

Releases epinephrine and norepinephrine (stimulate stronger/faster) heart beats

RAAS stimulates renal distal tubule to retain sodium and water

Increases production of vasopressin (anti-diuretic)

Kidneys increase sodium reabsorption, increasing blood volume, causing increased pressure within capillaries, resulting in edema formation

Heart muscle hypertrophy (increase muscle size)
Heart Failure - Treatment
Correct underlying disease (e.g., coronary artery disease, hypertension, dyslipidemia (high cholesterol/trigycerides), thyroid disease)
Bed rest when necessary
Sodium-restricted diet
Control symptoms with combination of drugs
Heart Failure - Goals
Reduce signs/symptoms associated with fluid overload

Increase exercise tolerance

Prolong life
Heart Failure - Drug Therapy
Vasodilators – reduce strain on left ventricle by reducing systemic vascular resistance (afterload)

Inotropic agents – boost cardiac output by stimulating the heart to increase force of contractions

Diuretics – enhance sodium and water excretion, reducing preload
Heart Failure - Nursing Assessment
Obtain history of heart disease, related cardiovascular diseases

Six cardinal signs of heart disease

Presence of altered cardiac function
Heart Failure - Diagnostic Tests
Echocardiogram

ECG
nuclear imaging studies
chest x-ray

laboratory tests
Heart Failure - Related diseases and causes
Related diseases

hypertension, hyperlipidemia, diabetes mellitus, lung disease.

Causes of systolic dysfunction

coronary artery disease
MI - if muscle damage
congestive heart failure
congenital heart disease
cardiomyopathy
Heart Failure - Six cardinal signs of heart disease
dyspnea - sob
chest pain,
fatigue
edema - swelling
syncope
palpitations - heart racing
Heart Failure - Digoxin - actions
Actions

Positive inotrope

Negative chronotropy
Digoxin - Uses
Treat moderate to severe systolic failure not responding to diuretics and ACE inhibitors

initial treatment for heart failure = ace and diuretics
Digoxin - Side effects
Digoxin toxicity

drowsiness, nausea/vomiting, loss of appetite (anorexia), diarrhea, disturbed color vision (yellow or green halos around objects), confusion, dizziness, agitation, and/or depression
Digoxin - notes
Always take the apical pulse for 1 full minute before administration; do not administer when heart rate is less than 60.

Maintenance dosing given daily.

Digoxin toxicity related to long half-life.

Digoxin immune Fab (ovine) (Digibind) is the antidote.
Heart failure drug - Inamrione & milrione - actions
Actions
vasodialtor and ionotrope

Increase the force and velocity of myocardial contractions
Heart failure drug -Inamrione & milrione - uses
Short-term management of systolic dysfunction heart failure in patients not responding adequately to digoxin, diuretics, or vasodilator therapy
Heart failure drug -Ace Inhibitors - actions
Actions
Reduce afterload by blocking angiotensin II-mediated peripheral vasoconstriction; reduce preload
Ace inhibitors - Uses
Treat mild to moderate systolic dysfunction heart failure
Beta Blockers - Actions
Actions
Inhibit cardiac response to sympathetic nerve stimulation; inhibit renin release
Beta blockers - uses
Uses
In combination with ACE inhibitors to treat heart failure
Natriuretic Peptides - drugs
Drug: nesiritide (Natrecor)
Natriuretic Peptides -Actions
Actions
Reduce preload and afterload pressures, increasing diuresis and sodium excretion
Suppress RAAS
Reduce secretion of norepinephrine
Natriuretic Peptides -uses
Uses
Treat severe heart failure
Natriuretic Peptides
Natriuretic peptide is a hormone normally secreted by the cardiac ventricles in response to fluid and pressure overload.
Ace inhibitors - Therapuetic outcome
Improved cardiac output with improved tissue perfusion; improved tolerance to exercise.
Heart Failure Drug therapay - therapuetic outcomes
Therapeutic outcomes: reduce systemic vascular resistance (afterload); reduce preload.
Heart failure - Facts
Affects an estimated 5 million Americans.
The number of other conditions that complicate its treatment increases as people live longer.
Diastolic dysfunction
heart fills during diastolic contraction but does not allow release of proper amount of blood.

If heart fills up too much blood backs up to the lungs

causes

pulmonary edema
wet cough
pulmonary congestion
stimulating factors to the sympathetic nervous system - all do the same thing
cathacolemines
epinephrine
norepineprine
sympathetic stimulate
sympathetic neuro transmitters
Left sided heart failure symptoms
reduced exercise tolerance, fatigue, dyspnea, weakness

cough, cardiac enlargement,

pulmonary crackles (water sounds in lungs)

elevated jugular venous pressure is positive ( neck veins are distended)

peripheral edema

S3 gallop rhythm - 3 heart sounds lub dub dub
Right sided heart failure symptoms
edema,
elevated jugular venous pressure,
S3 gallop over the right ventricle
often ascites or anasarca
Causes for Left sided heart failure - usually not pulmonary in nature
Ischemic heart disease (ST-segment elevation myocardial infarction (STEMI) is the most common cause of heart failure in the U.S.)
Hypertension (untreated or inadequately treated hypertension is the second most common cause of heart failure in the U.S.)
Arrhythmias (especially atrial fibrillation)
Valvular disease (aortic stenosis, aortic insufficiency, mitral insufficiency)
Cardiomyopathy
High-output states (anemia, hyperthyroidism)
Congenital heart disease
Volume overload (eg, in renal failure patients who miss dialysis)
Causes for Right sided heart failure - Usually pulmonary in nature
Chronic pulmonary disease (COPD)
Pulmonary embolism
Primary pulmonary hypertension
Valvular disease (mitral stenosis)