Chapter 33 Coronary Artery Disease and Acute Coronary Syndrome Flashcards
Coronary artery disease (CAD) is a type of blood vessel disorder that is included in the general category of atherosclerosis. The term atherosclerosis comes from two Greek words: athere, meaning “fatty mush,” and skleros, meaning “hard.”
1) This combination means that atherosclerosis begins as?
2) Consequently, atherosclerosis is commonly referred to as?
3) Although this disease can occur in any artery in the body, the atheromas (fatty deposits) prefer the?
4) The terms arteriosclerotic heart disease, cardiovascular heart disease, ischemic heart disease, coronary heart disease, and CAD all describe?
1) soft deposits of fat that harden with age.
2) “hardening of the arteries.”
3) coronary arteries.
4) This disease process.
Coronary Artery Disease
- Atherosclerosis-
- Inflammation and?
- CRP- c reactive protein
- Atherosclerosis- focal deposits of lipids and cholesterol intimal wall
- Tobacco use
- Hyperlipidemai
- Hypertension
- Diabetes
- Toxins
- Inflammation and endothelial injury
- CRP- c reactive protein
- Marker of inflammation
Atherosclerosis is the major cause of CAD. It is characterized by?
lipid deposits within the intima of the artery. Endothelial injury and inflammation play a central role in the development of atherosclerosis.
Etiology and Pathophysiology The endothelium (inner lining of the vessel wall) is normally nonreactive to platelets and leukocytes, as well as coagulation, fibrinolytic, and complement factors. However, the endothelial lining can be injured as a result of?
tobacco use, hyperlipidemia, hypertension, toxins, diabetes, hyperhomocysteinemia, and infection causing a local inflammatory response
What can cause chronic endothelial injury (Stage 1)?
- HTN
- Tobacco use
- Hyperlipidemia
- Hyperhomocysteinemia
- Diabetes
- Infections
- Toxins
Explain the fatty streak of the endothelial vessel wall (Stage 2)
Lipids accumulate and migrate into smooth muscle cells
Explain the fibrous plaque stage of endothelial injury/damage (Stage 3)
- Collagen covers the fatty streak
- Vessel lumen is narrowed
- Blood flow is reduced
- Fissures can develop
Explain the complicated lesion (Stage 4)
- Plaque rupture
- Thrombus formation
- Further narrowing or total occlusion of vessel
Pathogenesis of atherosclerosis.
A, Damaged endothelium
B, Fatty streak and lipid core formation
C, Fibrous plaque. Raised plaques are visible: some are yellow; others are white
D, Complicated lesion: thrombus is red; collagen is blue. Plaque is complicated by red thrombus deposition
C-reactive protein (CRP), a?
- protein produced by the liver
- nonspecific marker of inflammation
- increased in many patients with CAD
- levels rise when there is systemic inflammation.
- Chronic elevations linked with unstable plaques and oxidation of low-density lipoprotein (LDL) cholesterol.
Arteries
- Arteries supply blood to?
- Blockage or narrowing creates?
- Right coronary artery
- Left anterior descending
- Circumflex
- Arteries supply blood to myocardium
- Blockage or narrowing creates ischemia or necrosis
- Right coronary artery
- Right ventricle
- Inferior Surface
- Left anterior descending
- Septum
- Anterior left ventricle
- Circumflex
- Lateral Left ventricle
- Posterior surface
Risks unmodifiable and modifiable
1) Unmodifiable
- Age
- Gender
- Ethnicity
- Family
- Genetics
2) Modifiable
- Serum Lipids, Diabetes
- Blood pressure, Elevated homocysteine
- Smoking, Psychological state
- Obesity, physical activity
Nonmodifiable Risk Factors
- Increasing age
- Gender (more common in men than in women until 75 yr of age)
- Ethnicity (more common in white men than in African Americans)
- Genetic predisposition and family history of heart disease
Modifiable Risk Factors
Major & Contributing
1) Major • Serum lipids: • Total cholesterol >200 mg/dL • Triglycerides ≥150 mg/dL* • LDL cholesterol >160 mg/dL • HDL cholesterol <40 mg/dL in men or <50 mg/dL in women* • BP ≥140/90 mm Hg* • Diabetes • Tobacco use • Physical inactivity • Obesity: Waist circumference ≥102 cm (≥40 in) in men and ≥88 cm (≥35 in) in women* 2) Contributing • Fasting blood glucose ≥100 mg/dL* • Psychosocial risk factors (e.g., depression, hostility, anger, stress) • Elevated homocysteine levels
The incidence of CAD is highest among middle-aged men.
1) After age 75, the incidence of serious heart events in men and women equalizes, although CAD causes more deaths in?
2) Additionally, CAD is present in African American women at?
1) more deaths in women than men
2) rates higher than those of their white counterparts
highest incidence of coronary artery disease (CAD).
White men
CAD: African Americans
- African Americans have an early age of onset of CAD.
- Deaths from cardiovascular diseases (e.g., CAD, stroke) are higher for African Americans than for the overall population in the United States.
- African American women have a higher incidence and death rate related to CAD than white women.
CAD: Native Americans
- Native Americans die from heart disease earlier than expected. Mortality rates for those under 65 yr old are twice as high as those of other Americans.
- Major modifiable cardiovascular risk factors for Native Americans are tobacco use, hypertension, obesity, and diabetes.
CAD: Hispanics
- Hispanics have slightly lower rates of CAD than either non-Hispanic whites or African Americans.
- Hispanics have lower death rates from CAD than non-Hispanic whites.
Collateral Circulation.
Normally some arterial anastomoses or connections, called collateral circulation, exist within the coronary circulation.
1) Two factors contribute to the growth and extent of collateral circulation:
2) When plaque blocks the normal flow of blood through a coronary artery and the resulting ischemia is chronic, what happens?
3) When blockages in coronary arteries occur slowly over a long period, there is a greater chance of?
4) However, with rapid-onset CAD (e.g., familial hypercholesterolemia) or coronary spasm, time is inadequate for?
1) factors contribute to the growth and extent of collateral circulation:
- (1) inherited predisposition to develop new blood vessels (angiogenesis)
- (2) presence of chronic ischemia.
2) increased collateral circulation develops.
3) collateral circulation developing, and the heart muscle may still receive an adequate amount of blood and O2
4) collateral development. Consequently, a reduced blood flow results in a more severe ischemia or infarction.
CAD: Men • First heart event for men is more often? • Men report more typical? • Men receive more what than women? • Mortality rates from CAD have?
- Ml than angina.
- signs and symptoms of angina and MI.
- Men receive more evidence-based therapies (e.g., aspirin, statins, diagnostic catheterization, PCI) when acutely ill from CAD (e.g., MI) than women.
- decreased more rapidly for men than women.
CAD: Women
• Women experience the onset of heart disease approximately?
• CAD is the leading cause of?
• More women with MI (compared to men with MI) die of?
• Before menopause, women have?
- 10 yr later than men.
- death for women, regardless of race or ethnicity.
- sudden cardiac death before reaching the hospital.
- higher HDL cholesterol levels and lower LDL cholesterol levels than men. After menopause LDL levels increase
Acute coronary syndrome: Men
• After age 75, the incidence of MI in men and women?
• Men present more frequently than women with an?
• Men develop greater?
• Men have larger-diameter coronary arteries than women. Vessel diameter is inversely related to?
• Standard screening for risk of sudden cardiac death (e.g., EP studies) is?
- equalizes.
- acute MI as the first manifestation of CAD.
- collateral circulation than women.
- risk of restenosis after interventions.
- more predictive in men.
Acute coronary syndrome: Women
• Women are older than men when seen with?
• Women seek medical care later in the?
• First heart event for women is more often?
• Once a woman reaches menopause, her risk for?
• Fewer women than men manifest the?
• Fatigue is often the first symptom of?
• Women experience more “silent”?
• Among those who have an MI, women are more likely to suffer a?
• Women report more disability after?
• Women who have coronary artery bypass graft surgery have a?
- first MI and often have more co-morbidities.
- CAD process and often are more ill on presentation than men.
- unstable angina than MI.
- MI quadruples.
- “classic” signs and symptoms of UA or MI.
- ACS in women.
- MIs compared with men.
- fatal heart event within 1 yr than men.
- a heart event than men.
- higher mortality rate and more complications after surgery than men.
Gender Men vs Women
- Men
- 10-15 years earlier than women
- MI vs Angina
- Big ventricle
- Classic symptoms
- Acute MI- first evidence of CAD
- Better collateral circulation
- Women
- More deaths
- Fatigue
- Menopause
- Palpitations
- Often not treated as quickly.
- Symptoms not classic-Silent MI
- Higher mortality with CABG
An elevated serum lipid level is one of the four most firmly established risk factors for CAD. The risk of CAD is associated with a serum cholesterol level greater than?
- or a fasting triglyceride level greater than?
- serum cholesterol level greater than 200 mg/dL (5.2 mmol/L)
- fasting triglyceride level greater than 150 mg/dL (3.7 mmol/L)
LDL Cholesterol- more cholesterol
What are the levels?
1) <100 Optimal or < 70 for very high risk
2) 100-129 Near optimal/above optimal
3) 130-159 Borderline high
4) 160-189 High
5) 190 Very high
Total Cholesterol- Risk for level > 200 mg/dl
What are the levels?
1) <200 Desirable
2) 200-239 Borderline high
3) 240 High
HDL Cholesterol- more protein
What are the levels?
1) <40 Low, Women should be > 50
2) 60 High
Serum lipids: For lipids to be used and transported by the body, they must become soluble in blood by combining with proteins. Lipids combine with proteins to form lipoproteins. Lipoproteins are vehicles for fat mobilization and transport and vary in composition. Three major lipoproteins are?
high-density lipoproteins (HDLs), LDLs, and very-low-density lipoproteins (VLDLs).
HDLs contain more protein by weight and fewer lipids than any other lipoprotein. What is the function of HDLs?
HDLs carry lipids away from arteries and to the liver for metabolism. This process of HDL transport prevents lipid accumulation within the arterial walls. Therefore high serum HDL levels are desirable and lower the risk of CAD.
There are several types of HDLs. They differ by their density and apolipoprotein composition. Apolipoproteins are found on lipoproteins and activate enzyme or receptor sites that promote the removal of fat from plasma. Several types of apolipoproteins exist (e.g., apo A-I, apo B-100, apo C-I). Women have more apo A-I than men, and premenopausal women have HDL levels approximately three times greater than men. This is thought to be related to the protective effects of natural estrogen. After menopause, women’s HDL levels decrease and quickly near those of men. In general, HDL levels are?
higher in women, decrease with age, and are low in individuals with CAD. Physical activity and moderate alcohol intake increase HDL levels.
1) LDLs contain more?
2) VLDLs contain both?
3) Elevated LDL levels correlate closely with an increased incidence of?
1) cholesterol than any of the lipoproteins and have an attraction for arterial walls.
2) cholesterol and triglycerides and may deposit cholesterol directly on the walls of arteries.
3) atherosclerosis and CAD. Therefore low serum LDL levels are desirable
Certain diseases (e.g., type 2 diabetes, chronic kidney disease), drugs (e.g., corticosteroids, hormone therapy), and genetic disorders have been associated with elevated triglyceride levels.
1) Lifestyle factors that can contribute to elevated triglycerides include?
2) When a high triglyceride level is combined with a high LDL level, what happens?
1) high alcohol intake, high intake of refined carbohydrates and simple sugars, and physical inactivity.
2) a smaller, denser LDL particle is formed, which favors deposition on arterial walls. People with insulin resistance often have this pattern.
Guidelines for treating elevated LDL cholesterol are based on a person’s 10-year and lifetime risk for having heart disease or stroke. The following data generate a risk score:
(1) age
(2) gender
(3) race
(4) use of tobacco
(5) diabetes
(6) systolic BP
(7) diastolic BP
(8) use of BP drugs
(9) total cholesterol level
(10) HDL cholesterol level
individuals with no or only one risk factor are considered at low risk for the development of CAD, and their LDL goal is less than?
- Those at very high risk for developing CAD have multiple risk factors. They have an LDL goal of less than 70 mg/dL (1.8 mmol/L).7
- 160 mg/dL (4.14 mmol/L).
- less than 70 mg/dL (1.8 mmol/L)
Lipids:
- HDL Cholesterol- more protein
- Triglycerides-
- HDL Cholesterol- more protein
- <40 Low, Women should be > 50
- 60 High
- Triglycerides-
- fasting > 150 mg/dl associated with coronary artery disease.
LDL
- You want it?
Low (lower than 100 mg/dL) or it will lower you to the ground
HDL
- You want it?
High (greater than 40 mg/dL) for patient to feel healthy and high on life
A complete lipid profile is recommended every 5 years beginning at age 20. Guidelines recommend the following groups of people receive statin therapy:
(1) patients with known CVD
(2) patients with primary elevations of LDL cholesterol levels greater than or equal to 190 mg/dL (e.g., familial hypercholesterolemia)
(3) patients between 40 and 75 years old with diabetes and LDL cholesterol levels between 70 and 189 mg/dL
(4) patients between 40 and 75 years old with LDL cholesterol levels between 70 and 189 mg/dL and a 10-year risk for CVD of at least 7.5%
Lipid lowering drug therapy: Treatment also includes weight loss (if overweight), decreased dietary fat and cholesterol intake, and increased physical activity. Serum lipid levels should be reassessed after?
6 weeks of therapy. If they remain elevated, changes in drug therapy and additional dietary options should be considered.
Lipid lowering drugs:
1) Statins: Block synthesis of cholesterol, increase LDL receptors-hepatic
* Monitor Liver, CK
2) Niacin: Inhibits VLDL, LDL-flushing
* Take ASA or NSAID
3) Fibric Acid Derivatives- Lower triglycerides
* Increase HDLs
4) Bile acid sequestrants: bind with bile salts
* Interfere with medications
HMG-CoA Reductase Inhibitors (Statins) (Restrict Lipoprotein Production)
1) Mechanism of Action
2) Side Effects
3) Nursing Considerations
1) Mechanism of action: Block synthesis of cholesterol and increase LDL receptors in liver
- ↓ LDL
- ↓ Triglycerides
- ↑ HDL
2) Side Effects: Rash, GI disturbances, elevated liver enzymes, myopathy, rhabdomyolysis
3) Nursing Considerations: Well tolerated with few side effects. Monitor liver enzymes and creatine kinase (if muscle weakness or pain occurs).
Niacin (Restrict Lipoprotein Production)
1) Mechanism of Action
2) Side Effects
3) Nursing Considerations
1) Mechanism of Action: Inhibits synthesis and secretion of VLDL and LDL
- ↓ LDL
- ↓ Triglycerides
- ↑ HDL
2) Side Effects: Flushing and pruritus in upper torso and face, GI disturbances (e.g., nausea and vomiting, dyspepsia, diarrhea), orthostatic hypotension, elevated homocysteine levels
3) Nursing Considerations: Most side effects subside with time. Decreased liver function may occur with high doses.
Taking aspirin or NSAID 30 min before drug may prevent flushing. Take drug with food.
Treat elevated homocysteine levels with folic acid.
Fibric Acid Derivatives (Restrict Lipoprotein Production)
1) Mechanism of Action
2) Side Effects
3) Nursing Considerations
1) Mechanism of Action: Decrease hepatic synthesis and secretion of VLDL. Reduce triglycerides by ↓ VLDL
- ↓ LDL
- ↓ Triglycerides
- ↑ HDL
2) Side Effects: Rashes, mild GI disturbances (e.g., nausea, diarrhea), elevated liver enzymes
3) Nursing Considerations: May ↑ effects of warfarin (Coumadin) and some antihyperglycemic drugs.
When used in combination with statins, may increase adverse effects of statins, especially myopathy.
Bile-Acid Sequestrants (Increase Lipoprotein Removal)
1) Mechanism of Action
2) Side Effects
3) Nursing Considerations
1) Mechanism of Action: Bind with bile acids in intestine, forming insoluble complex and excreted in feces
Binding results in removal of LDL and cholesterol
↓ LDL
2) Side Effects: Unpleasant quality to taste, GI disturbances (e.g., indigestion, constipation, bloating)
3) Nursing Considerations: Effective and safe for long-term use. Side effects diminish with time.
Interfere with absorption of many drugs (e.g., digoxin, thiazide diuretics, warfarin, some antibiotics [e.g., penicillins])
Niacin (Niaspan)
- Instruct patient that flushing (especially of face and neck) may occur within 20 minutes after taking drug and may last for 30 to 60 minutes.
- Patient can premedicate with aspirin 30 minutes before taking to reduce flushing.
- Use of extended-release niacin may decrease side effects.
Antiplatelet Therapy
Aspirin is recommended for most people at risk for CVD. 1) Low-dose aspirin (81 mg) is recommended for adults?
2) For adults 60 to 69 years old who have a calculated?
3) Adults who have no contraindications (e.g., history of stroke), have a life expectancy of at least 10 years, and are willing to take low-dose aspirin daily for at least 10 years are more likely to benefit. Currently there is insufficient evidence to recommend low-dose aspirin for?
1) 50 to 59 years old who have a calculated 10-year CVD risk of 10% or more, are not at increased risk for bleeding (e.g., history of GI bleeding), have a life expectancy of at least 10 years, and are willing to take low-dose aspirin for at least 10 years.
2) 10-year CVD risk of 10% or more, the decision to take low-dose aspirin is an individual one.
3) those younger than 50 or older than 70
Antiplatelets
- Low dose aspirin-
- Plavix- What is this drug?
- Low dose aspirin-
- Plavix- prevent platelets in your blood from sticking together and forming a blood clot. Unwanted blood clots can occur with certain heart or blood vessel conditions.
used to prevent blood clots after a recent heart attack or stroke, and in people with certain disorders of the heart or blood vessels.
Chronic Stable Angina
CAD is a chronic and progressive disease. Patients may be asymptomatic for many years or may develop chronic stable chest pain. When the demand for myocardial O2 exceeds the ability of the coronary arteries to supply the heart with O2, myocardial ischemia occurs.
1) Angina, or chest pain, is the clinical manifestation of myocardial ischemia. It is caused by?
2) The most common reason for angina to develop is?
3) For ischemia secondary to atherosclerotic plaque to occur, the artery is?
1) either an increased demand for O2 or a decreased supply of O2.
2) narrowing of one or more coronary arteries by atherosclerosis. This leads to insufficient blood flow to the heart muscle.
3) usually blocked (stenosed) 70% or more (50% or more for the left main coronary artery)
Chronic stable angina refers to chest pain that occurs intermittently over a long period of time with a similar pattern of onset, duration, and intensity of symptoms.
1) It is often provoked by?
2) When asked, some patients may deny feeling pain but describe a?
3) Chronic angina pain usually does not change with?
1) physical exertion, stress, or emotional upset.
2) pressure, heaviness, or discomfort in the chest. This discomfort is often described as a squeezing, heavy, tight, or suffocating sensation. It may be associated with other symptoms such as dyspnea or fatigue.
3) position or breathing and is rarely described as sharp or stabbing.
ANGINA: Although most angina pain occurs substernally, it may radiate to other locations, including the jaw, neck, shoulders, and/or arms. Many people with angina complain of indigestion or a burning sensation in the epigastric region. The sensation may also be felt between the shoulder blades. Often people who complain of pain between the shoulder blades or indigestion type pain dismiss it as not being heart related. Some patients, especially women and older adults, report?
atypical symptoms of angina including dyspnea, nausea, and/or fatigue.4 This is referred to as angina equivalent.
Chronic Stable Angina:
1) The pain of chronic stable angina usually lasts for?
2) Pain at rest is unusual and often a symptom of?
3) A 12-lead electrocardiogram (ECG) often shows?
1) only a few minutes and commonly subsides when the precipitating factor is resolved (e.g., resting, calming down, using sublingual nitroglycerin (SL NTG) (Nitrostat). 2) UA.
3) ST segment depression and/or T wave inversion indicating ischemia. The ECG returns to baseline when the pain is relieved.
Chronic stable angina is controlled with drugs on an outpatient basis. Because chronic stable angina is often predictable, drugs are timed to?
provide peak effects during the time of day when angina is likely to occur. For example, if angina occurs when rising, the patient can take medication as soon as awakening and wait 30 minutes to 1 hour before engaging in activity.
PQRST Assessment of Angina P: Precipitating events Q: Quality of pain R: Region (location) and radiation of pain S: Severity of pain T: Timing
- P: What events or activities precipitated the pain or discomfort (e.g., argument, exercise, resting)?
- Q: What does the pain or discomfort feel like (e.g., pressure, dull, aching, tight, squeezing, heaviness)?
- R: Can you point to where the pain or discomfort is located? Does the pain or discomfort radiate to other areas (e.g., back, neck, arms, jaw, shoulder, elbow)?
- S: On a scale of 0 to 10, with 0 indicating no pain and 10 being the most severe pain you could imagine, what number would you give the pain or discomfort?
- T: When did the pain or discomfort begin? Has it changed since this time? Have you had pain/discomfort like this before?
Chronic stable angina
- Etiology
- Characteristics
- Etiology: Myocardial ischemia (usually secondary to CAD) caused by an O2 supply/demand mismatch
-Charactertistics:
• Episodic pain lasting a few minutes
• Provoked by exertion or stress
• Relieved by rest or nitroglycerin
Prinzmetel’s Angina
- Etiology
- Characteristics
- Etiology: Coronary vasospasm
- Characteristics:
• Occurs primarily at rest
• Triggered by smoking and increased levels of some substances (e.g., histamine, epinephrine, cocaine)
• May occur in presence or absence of CAD
Chronic Stable Angina main points
- Coronary arteries can’t meet demands for oxygen
- Reversible myocardial ischemia
- Intermittent, same pattern
- Constrictive, heavy
- No change with position or breathing.
- Pain subsides with rest
Stable Angina main points
- Sensation of choking
- Heaviness, weakness or numbness of upper extremities
- Dizziness
- Dyspnea
- Indigestion or nausea
clopidogrel (Plavix)
• Inhibits?
• Alternative for patients who cannot?
• Used to treat?
- Inhibits platelet aggregation
- Alternative for patients who cannot take aspirin
- Used to treat ACS with medical therapy alone or used in combination with aspirin after PCI for chronic stable angina or ACS
The treatment of chronic stable angina aims to decrease O2 demand and/or increase O2 supply. The reduction of risk factors is a priority and should include those strategies discussed for patients with CAD (see pp. 707-712). In addition to antiplatelet and lipid-lowering drug therapy, the most common therapeutic interventions for the management of chronic stable angina are the use of nitrates, angiotensin-converting enzyme (ACE) inhibitors, β-blockers, and calcium channel blockers to optimize myocardial perfusion
The treatment of chronic stable angina aims to decrease O2 demand and/or increase O2 supply. The reduction of risk factors is a priority and should include those strategies discussed for patients with CAD (see pp. 707-712). In addition to antiplatelet and lipid-lowering drug therapy, the most common therapeutic interventions for the management of chronic stable angina are the use of nitrates, angiotensin-converting enzyme (ACE) inhibitors, β-blockers, and calcium channel blockers to optimize myocardial perfusion
The treatment of chronic stable angina aims to decrease O2 demand and/or increase O2 supply. The reduction of risk factors is a priority. In addition to antiplatelet and lipid-lowering drug therapy, the most common therapeutic interventions for the management of chronic stable angina are the use of?
nitrates, angiotensin-converting enzyme (ACE) inhibitors, β-blockers, and calcium channel blockers to optimize myocardial perfusion
Strategies for the patient with chronic stable angina should address all the treatment elements and related patient teaching in the following mnemonic:
Element Treatment A B C D E F
Element Treatment
A Antiplatelet/anticoagulant therapy
Antianginal therapy
ACE inhibitor/angiotensin receptor blocker
B β-blocker
BP control
C Cigarette smoking cessation
Cholesterol (lipid) management
Calcium channel blockers
Cardiac rehabilitation
D Diet (weight management)
Diabetes management
Depression screening
E Education
Exercise
F Flu vaccinationNitrates function
- Promote peripheral vasodilation, decreasing preload and afterload
- Promote coronary artery vasodilation
- May prevent or control coronary vasospasm
β-Adrenergic Blockers function
- Inhibit sympathetic nervous stimulation of the heart
- Reduce heart rate, contractility, and BP
- Reduce ischemia
- Decrease afterload
Calcium Channel Blockers function
- Prevent calcium entry into vascular smooth muscle cells and myocytes (cardiac cells)
- May prevent or control coronary vasospasm
- Promote coronary and peripheral vasodilation
- Reduce heart rate, contractility, and BP
Short-acting nitrates are first-line therapy for the treatment of angina. Nitrates produce their principal effects by the following mechanisms:
1) Dilating peripheral blood vessels:
2) Dilating coronary arteries and collateral vessels:
1) Dilating peripheral blood vessels: This results in decreased SVR, venous pooling, and decreased venous blood return to the 716heart (preload). Therefore myocardial O2 demand is decreased because of the reduced cardiac workload.
2) Dilating coronary arteries and collateral vessels: This may increase blood flow to the ischemic areas of the heart. However, when the coronary arteries are severely atherosclerotic, coronary dilation is difficult to achieve.
Short acting nitrates: Sublingual Nitroglycerin.
1) SL NTG or translingual spray (Nitrolingual) usually relieves pain in about?
2) The recommended dose of NTG is?
1) 5 minutes and lasts approximately 30 to 40 minutes.
2) one tablet taken sublingually (SL) or one metered spray on the tongue for symptoms of angina. If symptoms are unchanged or worse after 5 minutes, tell the patient or caregiver to repeat NTG every 5 minutes for a maximum of three doses and contact emergency response system (ERS) if symptoms have not resolved completely.
Short acting sublingual nitroglycerin
1) Instruct the patient in the proper use of NTG. It should be easily accessible to the patient at all times. The patient should store the tablets where?
2) Tablets are packaged in?
1) away from light and heat sources, including body heat, to protect them from degradation.
2) light-resistant bottles with metal caps. Once opened, the tablets lose potency, and should be replaced every 6 months.
