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132 Terms
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What are the side effects of Nitroglycerine and Isosorbide dinitrate
1. headache 2. Orthostatic hypotension 3. Reflex tachycardia secondary to lowering BP
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What are the nursing considerations for the (nitrates) Nitroglycerine and Isosorbide dinitrate?
1\.Assess HR, BP before administration
2. They are given sublingual tablets between cheeks and lip and gums. Do not swallow. Take one tab every 5 minutes. if pain continues call 911 3. No alcohol 4. Slow position changes(orthostatic hypotension) 5. Headaches are common, if no headache then NTG is not working 6. Creams and patches: Tolerence will develop if drug holiday is not provided 12hrs on and 12 hrs off
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What are the drug to drug interactions with Nitroglycerine and Isosorbide dinitrate?
1. Severe hypotension: CV collaspe 2. Do not mix with heparin because it causes decreased anticoagulation 3. Do not mix with lithium because it can cause lithium toxicity
Do not mix with fentanyl because it can cause severe hypotension increased fluid requirements
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What is the classification of Nitroglycerine and Isosorbide?
Nitrates
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What is angina?
A type of chest pain, pressure or discomfort because the heart is not receiving oxygen due to narrowed artery
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What are some angina management medications?
Nitrates
Beta blockers
Calcium channel blockers
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What do angina drugs do?
They lower the oxygen demand and they do not increase perfusion ( the passage of blood)
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What should the nurse do for patients who took Nitrates?
•Patient should sit down
•Administer every 5 minutes, until relief of pain, for a total of 3 doses → if pain persists, call 911
•Usually results in headache, flushing and dizziness
•Protect from light and heat
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What is ischemia?
When a part of your body is lacking blood or oxygen
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What is under Acute Coronary syndrome? U
Unstable angina, No ST- segment elevation and St segment elevation
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What is acute coronary syndrome? (ACS)
Any condition brought on by a __**sudden blockage of blood flow**__ to the heart
What is the difference between stable and unstable angina?
Stable angina basically there is little plaque and blood can still flow through but the patient may have some pain and it is less likely to rapture. Oxygen demand increases and low oxygen supply becomes which equal pain. This is provoked by physical or emotional stress, cold
Unstable angina basically the plaque is larger and is likely to rapture, blood can still flow. However it can rupture and end up causing a clot to form which can completely close up the artery and cause a heart attack.
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Why does Coronary heart disease not produce symptoms early?
The smaller collateral vessels increase in size when the larger coronary vessels are closed up and provide another route for blood and oxygen to flow. They develop the same time the plaque aka atherosclerosis changes are occuring
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What are the types of chronic ischemic heart disease
Stable angina- blood is able to flow but decreased
Varient angina aka princemetal- Spasms in the heart
Silent mycardial ischemia - No symptoms but elderly may feel short of breathe
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Where is stable angina less common?
right side
jaw
epigastrium
back
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What is angina variant or vasospastic aka prinzmetals angina? What are the causes?
1\.It is coronary artery spasms and not due to plaque. It occurs with rest, minimal physical and frequently at night. Dysrhythmias can occur, the person is usually aware and high sudden risk of death.
2\.SNS activation
Ca+ channel dysfunction
Imbalance of endothelial cell vasodilating/ constricting substances
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Which medication fall under the classification of Class IV- Calcium channel blockers? \**hint 2 categories* \*
Why are Nondihydropyridines diltiazem verapamil and Dihydropyridine nifedipine taken?
for stable and variant angina
for antihypertensive
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What are the actions of Nondihydropyridines diltiazem verapamil and Dihydropyridine nifedipine?
Reduction of automaticity in the SA node, delay of conduction through the AV node and reduction of myocardial contractility
Dilation of arterioles
Reduce myocardial oxygen demand
Decrease afterload, decrease work load of the heart
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What are the side effects of Nondihydropyridines diltiazem verapamil and Dihydropyridine nifedipine?
For cardiac: Bradycardia, AV block and heart failure
For PV: hypotension and peripheral edema
For GI: Constipation
Reflex tachycardia
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What are the nursing considerations for Nondihydropyridines diltiazem verapamil and Dihydropyridine nifedipine?
Assess HR and BP before administration
Prolongs PR
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What are the drug to drug considerations for Nondihydropyridines diltiazem verapamil and Dihydropyridine nifedipine?
Increased risk of digoxin toxicity, so do not mix with digoxin
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What medication falls under the classification of Class II- Beta Blockers and Antihypertensive?
Propranolol
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What is propranolol taken for?
Angina
post MI
for antiarrhythmic
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What action does propranolol do?
**Reduces PVR**
***Neg. inotrope - ↓ force of contraction**
***Neg. chronotrope - ↓ HR**
***Neg. dromotrope - ↓ rate of electrical conduction**
\ *** Reduce myocardial oxygen demand**
Have cardio protective property
Help control sympathetic nervous system
They vasodilate
Block SnS
Prolong the left ventricle filling time
Decrease diastole
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What are the side effects for **propranolol ?**
\*Cardiac - heart failure, AV block, and sinus arrest, **bradycardia**
\***Hypotension** can occur secondary to reduced cardiac output.
\*In patients with asthma, blocking beta2 receptors in the lung can cause **bronchospasm**
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What are the nursing considerations for **propranolol ?**
***Assess apical BP and HR prior to administration. Notify HCP if < 60 b/m**
\*Prolongs PR, bradycardia
*** Don’t use in pts with ↑ ICP or Cerebral Hemorrhage** – don’t want to dilate those veins and ↑ the pressure even more
\ \***Don’t use in pt’s w/anemia**
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What are the drug to drug interaction for propranolol
Because of its cardiac and pulmonary effects, propranolol is **contraindicated for patients with asthma,** **sinus bradycardia**, high-degree heart block, and heart failure.
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What are the types of Acute Coronary Syndrome (ACS)
Unstable angina( unstable ruptured plaque)
No- ST segment elevation: NSTEMI
ST-Segment elevation: STEMI
\
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True or false: Treatment is aimed at limiting the amount of myocardium( the muscle of the heart) that dies
TRUE
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What are the female symptoms
1\.Indigestion
2\.Fatigue
3\.Shortness of breath \~ dyspnea
4\.Pain described as "pressure"
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What are the symptoms of unstable angina?
•Symptoms
1\.Pain at rest (> 20 minutes)
2\.New onset
3\.More severe, prolonged, or frequent than previous angina symptoms
4\.__Does not respond to NTG or rest__
•
•A cardiac emergency – Call 911 and transport to a hospital
•
•Cannot differentiate unstable angina from a MI by symptoms or physical examination
•
•If the unstable angina does *not* progress to a MI, there will be no cardiac cell death
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True or false: An acute (AMI) leaves behind an area of scar tissue where the cardiac myocytes have died
TRUE
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Describe how unstable and stable plaque do?
**Stable plaque** causes a narrowing that restricts blood flow:
Increased oxygen demand **→** __**ischemia**__ in myocardial cells supplied
Characterized by __smaller lipid center and thicker fibrous cap__
Stable angina
\ But…Plaque may become **unstable** → rupture → clot formation → partial or complete occlusion of artery
Death of the cardiac cells downstream
Characterized by __large lipid center, inflammation and thin cap__
__**Infarction**__ **(death) of cells** – hence the name *myocardial infarction.*
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What are the pathologic changes in a MI (heart attack)
The degree depends on:
1. Location and degree of closure 2. Amount of heart tissue supplied by vessel 3. Duration of closure 4. Metabolic needs of the affected tissue 5. Degree of collateral circulation( alternate or back up blood vessels in your body that can take over when another vein becomes blocked or damaged)
\
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what are the Pathologic changes pt2?
•The zone of infarction will increase in size as time goes on.
•
•Necrotic myocardial cells are replaced with scar tissue
•
• Scar tissue cannot contract or conduct action potentials
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What are the 3 zones of changes in a heart attack?
1. Ischemia •Ischemic areas cease to function within minutes 2. Injury -Irreversible damage/ death to myocardial cells occurs within 20-40 minutes 3. Infraction: •Early reperfusion after onset of ischemia can prevent further ischemia and necrosis
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How is Non ST segment elevation myocardial infarction (NSTEMI) different from unstable angina or STEMI?
__Unstable angina__, plaque disruption but no thrombus or occlusion of the coronary artery, therefore no myocardial cell death (no MI). However, may progress to NSTEMI or STEMI.
\ __NSTEMI__, a thrombus partially occludes a coronary artery. Depending on the degree of occlusion and oxygen demand of downstream heart cells, there is myocardial cell death (an MI) but *insufficient* to produce ST segment elevations.
\ Basically unstable angina can progress to NSTEMI OR STEMI
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What do ST segment elevation (STEMI) indicate?
•ST segment elevations are indicative of myocardial damage or ischemia
\ •It may take some time (minutes to hours) for the changes to show up, and they may not be present in all EKG leads
\ •Characterized by necrosis and ischemia of cardiac tissue
\ •Area of infarction (necrosis) is determined by the coronary artery that is affected and by its distribution of blood flow
• Changes can occur over time, depending on duration of ischemia (extent & location)
\ • Changes may not be present in all leads – take 12-lead EKG
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**6-12 hours**
**Subcellular cyanosis, decreased temp**
**No healing**
\ 18-24 hours
Tissue color change pale to gray or brown
Inflammation, intercellular enzyme release
\ 2-4 days
Visible necrosis
Proteolytic enzymes remove debris, catecholamines, lipolysis and glycogenolysis increase glucose levels and FFAs to help myocardial recovery form anaerobic state
\ 4-10 days
Soft with fatty changes in center, hemorrhage in infarcted area
Debris cleared collagen matrix produced
\ 10-14 days
Weak, fibrotic scare with some revascularization
Healing continues but mushy and vulnerable to stress
A Coronary Stent is a tiny wire mesh tube used to prop open an artery during angioplasty. The stent stays in the artery permanently. The stent will also improve blood flow to the heart muscle and will relieve chest pain (angina).
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What is the **Emergency Pain Relief??**
Morphine Sulfate IV push (not on table)
**Veno-dilation**
**Reduces preload** & cardiac work
“Modest” arterial vasodilation
*Reduces afterload & cardiac work*
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what are the **Immediate Reperfusion:** \n **Pharmacologic Agents**
__**Anti-platelet drugs**__
****Aspirin** ASAP!**
Clopidogrel (Plavix)
IIb, IIIa inhibitors (Repro)
\ **Decrease platelet aggregation**
à Prevent thrombus formation
\ __**Anticoagulants**__
**Heparin, Warfarin**
Reduce fibrin production à Suppress clotting
\
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What are the “Super Aspirins” \n Glycoprotein IIb/IIIa Receptor Antagonists?
Group of drugs that used in ACS and PCI suites
$$$ 1,000/course
IV
Used to prevent ischemic events
Abciximab: monoclonal antibody receptor inhibitor
Tirofiban and Eptifibatide (Integrilin): non-antibody receptor inhibitors
**Strong anti-platelet action**
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What medication falls under the classification of Anti-platelet?
Aspirin
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What is aspirin for?
Thrombosis prevention in:
\*Ischemic stroke
\*TIA’s
\*Chronic stable angina
\***Unstable angina**
\*Coronary stenting
\***MI – acute, previous and prevention**
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What are the actions of aspirin?
**Suppresses platelet aggregation**
\*Irreversible suppression of cyclooxygenase COX **–** for the life of the platelet 7 – 10 days
***Prevent thrombus formation**
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What are the side effects for aspirin?
**GI Bleeding**
***Hemorrhagic stroke**
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What are the nursing considerations for aspirin?
Dose: may use 325mg po initially in acute event, then 81 mg/day.
\*Enteric coating may not prevent GI bleeding.
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What are the drug to drug interactions for aspirin?
**Contraindication: Recent GI bleed 6 weeks,**
**CVA within 2 years, thrombocytopenia,** aneurysm, intracranial neoplasm
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What medication falls under the classification of the anticoagulants?
Heparin and Warfarin
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What is warfarin for?
*****Thromboembolism prevention: DVT, stroke (A. Fib and prosthetic heart valves)
\*Reduce risk of TIA and MI
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What does warfarin do?
Suppresses coagulation by **decreasing production of Vitamin K dependent clotting factors.**
**(Vitamin K antagonist)**
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What is the side effect of warfarin?
**Hemorrhage**
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What are some nursing considerations for warfarin?
**Monitor INR: goal for most 2 – 3.**
\*PO: **onset slow, half-life long, 1.5-2 days**
\*NOT useful in emergencies
\*Plan to administer IV Vit. K for warfarin overdose, slowly.
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what are the drug to drug interactions for warfarin?
**Many drug-drug interactions: may increase or decrease anticoagulation effect (INR)**
\*Regulate Vitamin K intake in diet.
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What is heparin for?
PE and DVT
\*Prevent post-operative DVT
\*During open-heart surgery and dialysis
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What does heparin do?
**Suppresses formation of fibrin**
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What are the side effects for heparin?
**Hemorrhage**
\*Spinal/epidural hematoma
\*ITP – low platelets
\*Hypersensitivity
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What are the nursing considerations for heparin?
IV or SQ
***Onset rapid, half-life short, 1.5 hours**
***IV: Monitor PTT times, platelet count, signs of bleeding closely**
\*Plan to administer Protamine Sulfate for heparin overdose.
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What are drug to drug interactions for heparin?
NONE
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What is infection?
▰Invasion from disease causing agents
▰Infection -> inflammation
▰Factors -> Infectious disease
▰Communicability
▰Infectivity
▰Virulence
▰Pathogenicity
▰Portal of Entry
Toxigenicity
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What is infection?
▰Complex __non-specific__ response to injury
▰2nd line of defense
▰Does **NOT** mean infection
▰Purpose:
▰Minimize effects of injury
▰Facilitate healing
▰Remove damaged tissue
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What are the s/s of inflammation?
▰Heat
▰Pain
▰Redness
▰Swelling
▰Loss of function
▰Exudate
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What are the systemic s/s of inflammation?
▰Leukocytosis
▰Left shift
▰Fever
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What is HIV?
●Retrovirus that attacks CD4 T cells
●Retro because they replicate from RNA→DNA
●No cure, but can live into late 70s if compliant with drug therapy
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What is the difference between acute and symtomatic infection?
**Acute Infection:** 2-4 weeks after infection and manifests as flu-like symptoms. Patient is highly contagious
**Symptomatic Infection:** CD4 T cell count drops below 200 and patient is incredibly susceptible to infection
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What is the HIV “treatment” and it’s main “goal”?
**ART treatment** is expensive and in many cases can provide a good quality life into late 70s - early 80s (so long as patient is compliant)
\*Main treatment goal = get that CD4 count UP!
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What is the Prep medication for HIV?
**PrEP** is a type of prophylactic therapy for those at high risk of contracting HIV. It includes drugs in the Nucleotide/Nucleoside reverse transcriptase inhibitors (NRTIs) .
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what is the ART therapy associated wit hHIV medication?
**ART Therapy** is prescribed for patients already diagnosed with HIV. It is a multi-drug regimen that requires strict adherence in order to work. Includes various combinations of the anti-virals in your chart.
Typically ART is 3 drugs from at least 2 of the classes.
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What are the protease inhibitors medication for HIV
**Protease Inhibitors:** stop the enzyme protease from cutting the long chains of the virus so it can’t be assembled.
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What are the integrase inhibitors medication for HIV
**Integrase Inhibitors:** prevent HIV from inserting its DNA into the human cell’s DNA.
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What are the fusion inhibitors medication for HIV?
**Fusion Inhibitors:** stops HIV from entering the cell
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What are the CCR5 Antagonist medication for HIV?
**CCR5 Antagonist:** blocks one of the co-receptors on the cell surface
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What are the NRTIs medication for hiv?
**NRTIs:** need intracellular cell metabolism to function
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What are the NNRTIs medication for HIV?
**NNRTIs:** don’t need the intracellular cell metabolism to function
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What is vulvar disease?
•Function of the valves is to ensure __unidirectional__ flow of blood in the heart
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What are the dysfunction of the valves?
•Dysfunction of valves
• __Narrowing of valve opening__
à does not *open* properly = *Stenosis*
• __Distortion of the valve__
à does not *close* properly =*Regurgitation*
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What are valve defects?
Valve defects: heart murmurs resulting from turbulent flow thru valve
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What dysfunction of the valve due to?
Dysfunction due to:
•Congenital, trauma, ischemia, age, inflammation
•Aortic & Mitral most common
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What is stenosis?
•Valve does not open properly
•
• resistance to blood flow through the valve
•
• volume & work of the chamber that empties thru narrowed valve
•Ex. Left Atrium (LA) for mitral stenosis
•
•Produces distention in one chamber & impaired filling in another
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What is regurgitating?
•Valve does not close properly
•
•Permits backflow to occur when valve should be closed
•Ex. Blood flows back into left ventricle (LV) during diastole when aortic valve should be closed
•
•Produces distention & work demands on ejecting chamber
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What are the signs of Mitral Valve Prolapse?
•Most asymptomatic
•
•Usually, unknown cause
\ •Palpitations (awareness of the heartbeat) and dysrhythmias are common
•Dysrhythmias may produce light-headedness or fainting
•Mitral regurgitation may necessitate valve repair or replacement
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what is mitral stenosis?
•Incomplete opening of mitral valve during diastole
à Left atrium distention
& impaired left ventricle filling
•
•Resistance mitral valve
à Left atrium dilates à left atrium pressure
à pulmonary vasculature
à pulmonary congestion & pulmonary HTN
•
Symptoms of ¯ CO occur with exertion, or HR (¯ diastolic filling time
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What is Mitral Valve Regurgitation?
•Incomplete closure of the mitral valve
•
•During systole, part of left ventricle stroke volume goes forward into aorta & regurgitate blood flows back into left atrium
•
•Results in ¯ CO &/or pulmonary congestion
•
•Left ventricle enlarges due to in ventricular pressure
•
•Left atrium dilates due to extra volume
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What is the difference between acute and chronic Mitral Valve Regurgitation
•__**Acute**__
•Occur with MI
•Occur with infective endocarditis
•*Usually* bacterial infection of the inner lining of the heart affecting chambers
•
•__**Chronic**__
Well tolerated, asymptomatic, until left ventricle function becomes
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what is the Aortic Valve Stenosis?
• resistance to ejection of blood from the left ventricle into the aorta
•
• resistance à work of the left ventricle & ¯ volume of blood ejected into systemic circulation
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What is the Aortic Valve Regurgitation?
•Incompetent aortic valve
\ à backflow of blood to the left ventricle during diastole
•
à left ventricle volume due to left atrium & blood leaking back thru incompetent valve
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What is a UTI?
●Common bacterial infection
●Can occur in the bladder (cystitis) or in the urethra (urethritis)
●Can be reoccuring and become resistant to antibiotics.
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wHICH therapy is bets for antibiotics?
●Antibiotic therapy should be based on culture and sensitivity of the bacteria
Some risk factors for UTIs can include urinary catheter use whether that means infection upon insertion or prolonged catheter use, urinary stasis can be a risk factor, immobility, sexual activity and poor personal hygiene to name a few. In addition to antibiotics, we can tell our patients a warm compresses and sitz bath (I had to look this up, but it is where you put a sitz bowel in your toilet seat and let the infected area soak for a little), keeping the area clean, increasing fluid intake to wash out the area (avoid citrus and caffeine until the infection clears) and voiding right before and after sex.
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What happens if UTI left untreated?
●If not treated, can become an ascending UTI which can affect bladder, kidneys and get into the blood
●In older patients, confusion/irritability could be a Sx of UTI
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Which medications classification is under NSAIDS?
Aspirin
Ibuprofen (Advil and Mortin)
\
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What is aspirin for?
\*Fever
\ \*Anti-inflammation
Analgesic - pain
Reduction of platelet aggregation
Reduction of cancer risk
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What is the action of Aspirin?
Irreversible, non-selective inhibitor of COX (1 and 2)
\ \*Anti-inflammatory
\*Antipyretic
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What are the side effects of aspirin?
GI – gastritis, dyspepsia, ulcers
\ \*Bleeding
\ Renal impairment
Allergy
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What are the nursing consideration for aspirin?
Dose:
\ \*Antipyretic: 325-650mg po every 4 hours
Cardiac: may use 325mg po initially in acute event, then 81 mg/day.
\*Enteric coating may not prevent GI bleeding.
\*Administer with food
\*Avoid alcohol ingestion with medication
\*Drug-drug interactions/contraindications
\*Do not administer to children or adolescents due to risk of Reyes Syndrome