Module 4 Cardiovascular
N609

Primary or essential
Affects 95% of adults
Cause unknown; contributing factors are environmental and genetic
Secondary
5% of all hypertension; cause is identified
Idiopathic
No identifiable cause

Chronic kidney disease (CKD): anemia, low glomerular filtration rate, small kidney
Renovascular hypertension: abdominal bruit, elevated plasma renin activity, >30% elevation of creatinine with starting blood pressure (BP)-lowering agents, hypothyroidism
Hyperparathyroidism: elevated calcium
Pheochromocytoma
Sleep apnea
Primary aldosteronism: hypokalemia, ratio serum aldosterone/plasma renin activity >25:30

Oral contraceptives
Nicotine
Steroids
Appetite suppressants
Tricyclic antidepressants, the antidepressant venlafaxine (Effexor)
Cyclosporine (Sandimmune), nasal decongestants
Nonsteroidal anti-inflammatory drugs

Role of the nervous system
Role of the renal system

Joint National Committee guidelines for prehypertension and hypertension
Ambulatory BP monitoring (ABPM): recommended for patients with suspected variable BP
Physical examination
Diagnostic tests

Electrocardiogram
Blood glucose; hemoglobin, hematocrit
Complete chemistry panel especially serum potassium, calcium, and magnesium
Complete urinalysis, creatinine, estimated glomerular filtration rate
Liver function tests
Glycosylated hemoglobin (hemoglobin A1c) and fasting lipid panel (9- to 12-hour fast)

Manage hypertension.
Reduce cardiovascular disease (including lipid disorders, glucose intolerance or diabetes, obesity, and smoking) and renal disease.
Attain treatment goal of systolic blood pressure (SBP) less than 140 mm Hg and diastolic blood pressure (DBP) less than 90 mm Hg with special note of higher goals for older patients.

Maintain appropriate body weight (BMI of 19.5 to 24.9).
Adopt the Dietary Approaches to Stop Hypertension diet, USDA Food Pattern Diet, or the AHA diet.
Restrict dietary sodium to less than 2.4 g QD.
Increase physical activity.
Reduce alcohol consumption.

Classes
Carbonic anhydrase inhibitors (not used for hypertension because of their weak antihypertensive effects), thiazides, thiazide-like diuretics, loop diuretics, and potassium-sparing diuretics.
Action
Decrease BP by causing diuresis, which results in decreased plasma volume, stroke volume, and cardiac output; may cause hypokalemia.

Atenolol (Tenormin) 25-100 mg QD
Bisoprolol (Zebeta) 2.5-10 mg
Metoprolol tartrate (Lopressor) 50-100 QD-BID
Nadolol (Corgard) 40-120 mg QD
Propranolol (Inderal, Inderal LA) 40-160 mg BID 60-180 mg BID
Metoprolol succinate (Toprol-XL) 50-100 mg QD-BID
Acebutolol (Sectral) 200-600 mg BID

Benazepril (Lotensin) 10-40 mg QD-BID
Captopril (Capoten) 25-100 mg BID-TID
Fosinopril (Monopril) 10-40 mg QD
Lisinopril (Prinivil, Zestril) 10-40 mg QD
Moexipril (Univasc) 7.5-30 mg QD
Quinapril (Accupril) 10-80 mg QD
Ramipril (Altace) 2.5-20 mg QD
Trandolapril (Mavik) 1-4 mg QD

Losartan (Cozaar) 25-100 mg QD-BID
Valsartan (Diovan) 80-320 mg QD
Candesartan cilexetil (Atacand) 8-32 mg QD
Irbesartan (Avapro) 150-300 mg QD
Telmisartan (Micardis) 20-80 mg QD
Eprosartan (Teveten) 400-800 mg QD-BID
Olmesartan (Benicar) 20-40 mg QD

Nondihydropyridines
Diltiazem HC1 (Cardizem SR, Cardizem CD) (Dilacor XR) (Tiazac) 180-420 mg QD (Diltia XR) 120-480 mg QD
Verapamil HC1 (Isoptin SR, Calan SR, Verelan) 120-480 mg QD
Dihydropyridines
Amlodipine (Norvasc) 2.5-10 mg QD

Dihydropyridines (cont.)
Felodipine (Plendil) 2.5-20 mg QD
Isradipine (DynaCirc) 2.5-10 mg BID (DynaCirc CR) 5-10 mg BID
Nicardipine (Cardene SR) 60-120 mg BID
Nifedipine (Procardia XL) 30-60 mg QD
Nisoldipine (Sular) 10-40 mg QD

Doxazosin (Cardura) 1-16 mg QD
Prazosin (Minipress) 2-20 mg BID-TID
Terazosin (Hytrin) 1-20 mg QD-BID

Clonidine (Catapres) 0.1-0.8 mg BID-TID
Transdermal (Catapres TTS) one patch weekly (0.1-0.3 mg/d)
Guanabenz (Wytensin) 4-64 mg BID
Guanfacine (Tenex) 0.5-2.0 mg QD
Methyldopa (Aldomet) 250-1,000 mg BID

Hydralazine (Apresoline) 25-100 mg BID
Minoxidil (Loniten) 2.5-80 mg QD-BID

A practitioner is prescribing losartan (Cozaar) for a patient newly diagnosed with primary hypertension. What is an appropriate dose for this patient?
A. 25 mg QD-BID
B. 125 mg QD-bid
C. 320 mg QD
D. 32 mg QD

A. 25 mg QD-BID
Rationale: A starting dosage of losartan is 25 mg QD-BID. If goal is not reached, the drug can be titrated up to achieve maximum effectiveness.

A patient with hypertension is prescribed a thiazide diuretic. What type of supplement may this patient need?
A. Vitamin C
B. Calcium
C. Potassium
D. Vitamin D

C. Potassium
Rationale: As a result of drug-induced diuresis, hypokalemia occurs in 15% to 20% of patients taking low-dose thiazide diuretics; therefore, potassium supplements can be utilized by some patients.

Pediatric patients
Managed by the fourth report from the National High Blood Pressure Education Working Group for Hypertension Management Children and Adolescents.
Diagnosis based on the child's age and goal ranges of the SBP and/or DBP falls into percentiles.
Geriatric patients
TONE: in older patients with hypertension, BP can be reduced by low-sodium diets and weight loss.

Geriatric patients (cont.)
Older patients are very sensitive to medications that cause sympathetic inhibition and are at greater risk of becoming volume depleted than their younger patients.
Black patients
Old thought: High hypertension risk factors: low circulating renin levels with excessive levels of angiotensin II; endothelial dysfunction as a result of reduced bradykinin and nitric oxide; abnormal sympathetic nervous system activation; and higher levels of intracellular calcium stores.

Black patients
New info: ALLHAT trial found no significant differences in hypertensive outcomes between diuretics and CCBs in black patients
AHA and ACC no longer use race in their treatment algorithms for hypertension

Hypertension increases cardiovascular risks in diabetic patients.
Current guidelines recommend lowering BP to <140/90.
All patients should be encouraged to modify their lifestyle, to limit sodium intake, lose weight, and exercise for 150 minutes/week.
All major antihypertensive drug classes, renin-angiotensin-aldosterone systems (RAAS) blockers, beta-blockers, diuretics, and calcium blockers are useful in diabetic patients. Angiotensin-converting enzyme inhibitor (ACEI) and angiotensin II receptor blockers (ARBs) are recommended.

A practitioner is choosing an antihypertensive drug for a patient who has diabetes. What is considered the cornerstone of therapy for this patient?
A. Two RAAS blockers or the use of ACEI and an ARB in combination
B. ACEI and ARBs
C. RAAS blockers and diuretics
D. Diuretics alone

B. ACEI and ARBs
Rationale: All major antihypertensive drug classes, RAAS blockers, beta-blockers, diuretics, and calcium blockers are useful in diabetic patients. ACEI and ARBs are considered the cornerstone of therapy. Combination therapy consisting of two RAAS blockers or the use of ACEI and an ARB in combination is not recommended because of the risk of causing renal impairment, hypotension, and hyperkalemia.

Definition: extremely high SBP and/or DBP
Hypertensive emergency: end-organ damage is present
Goal: protect remaining end-organ function, reduce risk of complications, and improve outcomes
Hypertensive urgency: crisis without evidence of organ damage
Immediate treatment with intravenous antihypertensive agent(s) is needed to salvage viable tissue

Direct vasodilators (hydralazine)
Nitrates (sodium nitroprusside, nitroglycerin)
Calcium channel blockers (nicardipine, clevidipine)
Sympathoplegic agents (labetalol, esmolol)
Alpha-I blockers (phentolamine)
ACEIs (enalaprilat)

Importance of adhering to therapy
Consequences of uncontrolled hypertension
Side effects and actions to take to relieve them
Which adverse reactions to report to practitioner
Nutrition/lifestyle changes
Complementary and alternative medications (to date, there is no evidence that alternative medications reduce BP)

Hypertension is a complex chronic disease both in terms of pathophysiology and treatment.
Hypertension increases the risk for cardiovascular disease and CKD.
Heart disease is a prevalent cause of death in the United States, thus making management of a patient's BP crucial.
Successful treatment of high pressure can help prevent negative outcomes.

Definition: blood disorder characterized by elevations in blood cholesterol levels; one of the major contributing risk factors in the development of coronary heart disease (CHD).
Causes: increased level of any of the lipoproteins; in 95% of all those with hyperlipidemia, the cause is a combination of genetic and environmental factors.

Medications (e.g., beta-blockers and oral contraceptives)
Concomitant disease states or other conditions (e.g., diabetes mellitus and pregnancy)
Diets high in fat and cholesterol
Lack of exercise
Obesity
Smoking

Major plasma lipids: cholesterol, triglycerides, phospholipids.
Lipoproteins are produced in the liver and intestines, but endogenous production of lipoproteins occurs primarily in the liver.
Apolipoproteins: specialized proteins that identify specific receptors to which the lipoprotein will bind; they play a role in the development or prevention of hyperlipidemia by controlling the interaction and metabolism of the lipoproteins.

Chylomicrons: composed primarily of triglycerides
Very-low-density lipoproteins (VLDLs): composed of cholesterol and triglycerides; are the major carrier of endogenous triglycerides
Intermediate-density lipoproteins (IDLs): contains the most cholesterol by weight of all the lipoproteins
Low-density lipoproteins (LDLs): "bad" cholesterol
High-density lipoproteins (HDLs): "good" cholesterol

Coronary heart disease (ASCVD)
Myocardial infarction
Significant myocardial ischemia (angina pectoris)
History of coronary artery bypass graft
History of coronary angioplasty
Angiographic evidence of lesions

Peripheral vascular disease
Claudication
Carotid artery disease
Thrombotic stroke
Transient ischemic attack

In 2018, the American College of Cardiology (ACC) and the American Heart Association (AHA) released updated guidelines on the management of blood cholesterol.
Assessment of traditional ASCVD risk factors in patients age 20 to 79 without a history of CVD every 4 to 6 years. In addition to lipid levels, traditional risk factors include age, gender, systolic blood pressure, antihypertensive therapy use, presence of diabetes, and smoking status.
A full lipid panel, which also contains LDL cholesterol and triglycerides, should be obtained to fully evaluate a patient's ASCVD risk.

A coronary artery calcium (CAC) scan is a noninvasive procedure that detects atherosclerotic plaque burden (total plaque area and density).
The result of the CAC scan is characterized by the Agatston score.
The CAC score can assist clinicians and patients to further determine the ASCVD risk of an individual for future cardiovascular (CV) events and to determine whether statin therapy should be initiated or delayed.

Diet: high in fruits, vegetables, whole grains, low-fat dairy products, poultry, fish, legumes, nontropical vegetable oils, and nuts - with a healthy balance of macronutrients (protein, carbs, fat and water)
Exercise: aerobic physical activity three to four times a weeks, with each session averaging about 40 minutes
Weight loss
Moderation of alcohol intake
Smoking cessation

The ACC/AHA cholesterol guidelines recommend use of HMG-CoA reductase inhibitors (statins) for ASCVD prevention in four groups of patients, termed "statin benefit groups."
The statin benefit groups include individuals who (1) have clinical ASCVD (highest risk group) (2) do not have ASCVD but have severe hyperlipidemia defined as LDL-C >190 and are 20 to 75 years of age (high risk group) (3) are 40 to 75 years old with type 1 or type 2 diabetes mellitus and have LDL-C values of 70 to 189 mg/dL, or (4) are 40 to 75 years old with LDL-C values of 70 to 189 mg/dL and have a 10-year risk of ASCVD of >=7.5%.

Cholesterol levels should be repeated within 1 to 3 months after initiating treatment.
For individuals whose response is less than expected, providers should assess reasons such as nonadherence, including intolerance to the statin or affordability.
Lifestyle modifications should also be reemphasized.

A 50-year-old patient with type 1 diabetes and no ASCVD has an LDL-C value of 180. The ASCVD risk is <7.5%. What statin dosage would be appropriate for this patient?
A. Low-intensity statin
B. Moderate-intensity statin
C. High-intensity statin
D. No statin is recommended

B. Moderate-intensity statin
Rationale: For a patient with no ASCVD, who is 40 to 75 years old with type 1 or type 2 diabetes mellitus and has LDL-C values of 70 to 189 mg/dL, a statin is recommended. With an ASCVD risk <7.5%, a moderate-intensity statin is recommended, and with an ASCVD risk >=7.5%, a high-intensity statin is recommended.

The statins are well tolerated by most patients and long-term therapy does not appear to have any serious risks.
The most common complaint with statin use is muscle-related symptoms, including pain, tenderness, weakness, and fatigue.

A practitioner is prescribing a moderate-intensity dosage of Crestor for a 65-year-old patient with ASCVD. What dosage would be appropriate for this patient?
A. 60-80 mg
B. 40-60 mg
C. 20-40 mg
D. 5-10 mg

D. 5-10 mg
Rationale: A moderate-intensity dosage of rosuvastatin (Crestor) is 5-10 mg. 20-40 mg is a high-intensity dosage for Crestor.

Action: primarily block the conversion of HMG-CoA to mevalonate, which is the rate-limiting step in the production of cholesterol in the liver.
Maximum effects: usually are seen after 4 to 6 weeks of therapy. For this reason, dosage adjustments should not be made more frequently than every 4 weeks.
Contraindications: pregnant and lactating women, active liver disease, unexplained elevated aminotransferase levels, and heavy alcohol use.

Adverse events
Well tolerated by most patients; myopathies, gastrointestinal (GI) complaints, headache may occur
Interaction
Drugs that can also cause myopathy (e.g., cyclosporine, erythromycin, azole antifungals)

Only cholesterol absorption inhibitor on the market.
Dosage: 10 mg daily.
Action: acts at the brush border of the small intestine and inhibits the absorption of cholesterol, decreasing delivery of intestinal cholesterol to the liver. This causes a reduction of hepatic cholesterol stores and an increase in clearance of cholesterol from the blood.
Contraindications: hypersensitivity to components of the medicine, pregnancy, liver disease if used with statin.

Proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors are a novel class of monoclonal antibodies for LDL cholesterol lowering.
LDL receptors (LDLR) on the surface of hepatocytes play an important role in clearing LDL in the circulation.
PCSK9 regulates LDLR by binding to LDLR promoting its degradation and reducing the number of available LDLR available, hence, increasing circulating LDL cholesterol.
By inhibiting PCSK9, LDL cholesterol can significantly be lowered.

Action: decrease cholesterol absorption through the exogenous pathway; can decrease LDL cholesterol levels by 15% to 30%, increase HDL levels by approximately 3%, and increase triglyceride levels by up to 15%
Contraindications: fasting triglyceride levels >=300 mg/dL
Adverse events: GI related
Interactions: should be taken with food

naturally occurring B vitamin that can improve cholesterol levels when used at doses 100 to 300 times the recommended daily vitamin allowance
decrease VLDL synthesis in the liver, inhibit lipolysis in adipose tissue, and increase lipoprotein lipase activity
at least 1.5 g niacin daily, titrated gradually

Class of lipid-lowering drugs mainly affects triglyceride and HDL cholesterol levels.
Action: principal effect of triglyceride lowering appears to result from the stimulation of lipoprotein lipase, which enhances the breakdown of VLDL to LDL cholesterol.
Dosage: gemfibrozil given in 600-mg doses twice daily with breakfast and dinner.
Contraindications: gallstones, hepatic/renal dysfunction.

Similar to fibric acids, omega-3 fatty acids are not considered a major class of lipid-lowering drugs due to a lack of LDL cholesterol lowering.
In some cases, omega-3 fatty acids may increase HDL cholesterol levels.
Additionally, there have been no studies showing reduced CV morbidity and mortality.

Adenosine triphosphate-citrate lyase (ACL) inhibitors are the newest class of LDL cholesterol lowering medication on the market.
ACL is an enzyme upstream of HMG-CoA reductase in the cholesterol synthesis pathway.
Inhibition of ACL reduces cholesterol biosynthesis in the liver and subsequently decreases LDL cholesterol by upregulation of LDL receptors.

Rare genetic disorder characterized by dysfunctional LDL cholesterol receptors on the liver, which leads to severely elevated cholesterol levels (LDL cholesterol levels >60 mg/dL) and ASCVD at an early age.
In 2013, mipomersen and lomitapide were approved in the United States for the treatment of FH.
Two new medications, alirocumab (Praluent) and evolocumab (Repatha), which are monoclonal antibodies that target PCSK9 were approved by the Food and Drug Administration (FDA) in late 2015.

A practitioner is treating a patient with severe FH. What drug might the practitioner prescribe?
A. Alirocumab (Praluent)
B. Ezetimibe (Zetia)
C. Gemfibrozil (Lopid)
D. Niacin

A. Alirocumab (Praluent)
Rationale: Two new medications, alirocumab (Praluent) and evolocumab (Repatha), which are monoclonal antibodies that target PCSK9 were approved by the FDA in late 2015. Prior to that, mipomersen and lomitapide were approved in the United States for the treatment of FH in 2013.

Lovastatin/niacin (Advicor) and simvastatin/niacin (Simcor): statin/niacin and statin/gemfibrozil used together for patients with severely elevated LDL cholesterol, low HDL cholesterol, and hypertriglyceridemia.
Combining statins with a cholesterol absorption inhibitor has shown added benefits in both reducing LDL cholesterol and ASCVD event rates.
Bile acid resins can be used safely and effectively with statins, niacin, and fibric acid derivatives to enhance LDL cholesterol lowering.

Pediatric
Young adults
Geriatric
Women

Lifestyle changes
Regular laboratory tests

Hyperlipidemia is one of the major contributing risk factors in the development of CHD.
It is estimated that approximately 15.5 million people in the United States have CHD, with approximately 375,000 deaths each year (American Heart Association, 2015).
Numerous large studies have shown that reducing elevated cholesterol levels reduces morbidity and mortality rates in patients with and without existing CHD.

Chest pain
Discomfort
Heaviness or pressure
Sensation may radiate to the back, neck, jaw, and throat or arms.
Usually these sensations last 1 to 15 minutes.
Shortness of breath
Fatigue

Stable: The paroxysmal chest pain or discomfort is provoked by physical exertion or emotional stress and is relieved by rest and/or nitroglycerin (NTG).
Unstable: Experienced when the patient is at rest or if the episode is prolonged or progressive.
Preinfarction angina, crescendo angina, or intermittent coronary syndrome.
Variant angina, nocturnal angina, angina decubitus, and postinfarction angina.

Age
Heredity
Gender

Cigarette smoking
Hypertension
Dyslipidemia
Diabetes
Obesity
Physical inactivity

The fatty streak
Caused by the development of fatty, lipid-rich lesions that result from macrophages adhering to the intact endothelial surface.
The fibrous plaque
A white, elevated area on the surface of the artery that signals the beginning of progressive changes in the arterial wall, including protrusion of the lesion into the lumen of the artery.

The complicated lesion
Contains a fibrous plaque, calcium deposits, and a thrombus formed by hemorrhage into the plaque.
As the complicated lesion, with its lipid, necrotic center, becomes larger, it calcifies. The intimal surface may develop open or ruptured areas that degenerate into an ulcer and eventually become thrombus formation blocking the lumen of the artery and blood flow.
The result is cardiac ischemia and anginal symptoms.

A practitioner notes a fibrous plaque on a patient's artery. What development occurs during this stage of atherosclerosis?
A. The macrophages take in lipids, which leads to a thickening of the intimal layer.
B. Protrusion of the lesion into the lumen of the artery occurs.
C. Thrombus forms by hemorrhage into the plaque.
D. A blockage occurs impeding blood flow to the heart.

B. Protrusion of the lesion into the lumen of the artery occurs.
Rationale: In the fibrous plaque stage of atherosclerosis, the raised fibrous plaque signals the beginning of progressive changes in the arterial wall, including protrusion of the lesion into the lumen of the artery. In the fatty streak stage, the macrophages take in lipids, which leads to a thickening of the intimal layer. A thrombus forms by hemorrhage into the plaque and a blockage occurs impeding blood flow to the heart in the complicated lesion stage of atherosclerosis.

Narrowing of the coronary artery lumen
Arterial muscle spasm and limit of the blood supply to the myocardium
Thought to be smooth muscles of the coronary arteries contract in response to neurogenic stimulation

Causes
Ambient factors that increase myocardial oxygen demand
Circumstances that decrease oxygen supply
Treatment
Therapy is directed at resolution or control of these situations so that the heart can receive the oxygen it needs to meet the physical demands of the body.

Health history
Physical findings
Diagnostic tests
Electrocardiography, echocardiography, exercise tolerance testing, radioisotope imaging, and coronary artery angiography

Relieving the acute anginal episode
Preventing additional anginal episodes
Preventing progression of CHD
Reducing the risk of MI
Improving functional capacity
Prolonging survival and maintaining patient quality of life
Avoiding adverse events associated with therapy

Captopril (Capoten)
Start: 6.25 mg or 12.5 mg TID; therapeutic range: 25-100 mg TID
Enalapril (Vasotec)
Start: 2.5 mg qd or BID; range: 5-20 mg qd or BID daily
Fosinopril (Monopril)
Start: 10 mg qd; range: 10-40 mg qd

Lisinopril (Zestril, Prinivil)
Start: 5 mg qd; range: 5-20 mg qd
Quinapril (Accupril)
Start: 5 mg BID; range: 20-40 BID
Ramipril (Altace)
Start: 1.25 mg twice daily; range: 1.25-5 mg twice daily

Losartan (Cozaar)
Start: 12.5 mg/day; range: 50-100 mg/d
Valsartan (Diovan)
Start: 80 mg/d; range: 80-160 mg twice daily

Nitroglycerin (Nitrostat, NitroQuick)
0.4 mg SL prn
Isosorbide dinitrate (ISDN; Isordil, Sorbitrate)
5 mg SL prn

Nitroglycerin
Topical ointment (Nitro-BID) 12-1 in BID-TID
Transdermal patch (Minitran, Nitro-Dur, Nitrol, Transderm-Nitro) 0.2-0.8 mg/h
Isosorbide mononitrate (ISMN)
Immediate release (Ismo, Monoket) 5-20 mg BID
Extended release (Imdur) 30-120 mg BID

Propranolol
Immediate release (Inderal) 40-160 mg BID
Extended release (Inderal LA) 80-240 mg qd
Atenolol (Tenormin) 25-100 mg qd
Metoprolol
Immediate release (metoprolol tartrate, Lopressor) 25-200 mg TID; extended release (metoprolol succinate, Toprol XL) 50-100 mg qd

Amlodipine (Norvasc) 2.5-10 mg qd
Nifedipine (extended release, Adalat CC, Procardia XL) 30-60 mg qd
Diltiazem (extended release, Cardizem CD, Dilacor XR, Tiazac) 180-420 mg qd
Verapamil
Immediate release (Calan, Isoptin) 80-320 mg BID; extended release (Calan SR, Isoptin SR) 120-480 mg qd

Aspirin
81-325 mg qd
Clopidogrel (Plavix)
75 mg qd
Ranolazine (Ranexa) 500-1,000 mg qd

A practitioner is prescribing a calcium channel blocker for a patient experiencing angina. What might the practitioner prescribe?
A. Propranolol
B. Nitroglycerin
C. Captopril
D. Amlodipine

D. Amlodipine
Rationale: Amlodipine is a calcium channel blocker, propranolol is a beta-blocker, nitroglycerin is a long-lasting nitrate, and captopril is an angiotensin-converting enzyme inhibitor.

Fibrinolytic therapy should only be utilized in the management of STEMI, as this class of medications has no role in the treatment of NSTEMI.
These agents are only used in the patient who is unable to receive PCI as reperfusion therapy.

Acute treatment of anginal episodes
Chronic prevention of anginal episodes
Treatment selection in acute coronary syndromes
Acute treatment of myocardial infarction
Maintenance therapy

A practitioner is treating a patient with newly diagnosed angina. What is the first line of treatment for this patient?
A. Short-acting nitrate
B. Long-acting nitrate
C. Beta-blocker
D. Calcium channel blocker

A. Short-acting nitrate
Rationale: The first-line recommended order of treatment for angina for all patients is short-acting nitrate and aspirin. The first-line recommended order of treatment for patients with chronic angina episodes is a beta-blocker or calcium channel blocker.

Stress test
ECG
Routine follow-up depending on the frequency and severity of patient complaints
Vital signs taken at each office visit
Monitoring parameters determined by the drug regimen

Drug information
Patient-oriented information sources
Complementary and alternative medications

Angina is a syndrome-a constellation of symptoms-that results from myocardial oxygen demand being greater than the oxygen supply (myocardial ischemia).
By definition, angina is associated with reversible ischemia, so it does not result in permanent myocardial damage.
Nonpharmacologic therapy is the cornerstone of treatment for patients with angina. The practitioner must assess the patient's modifiable risk factors and work with them to reduce the risk for CHD.

Most common causes: coronary artery disease, hypertension, and idiopathic cardiomyopathy
Acute conditions that may result in heart failure (HF): acute MI, arrhythmias, pulmonary embolism, sepsis, and acute myocardial ischemia
Gradual development of HF: may be caused by liver or renal disease, primary cardiomyopathy, cardiac valve disease, anemia, bacterial endocarditis, viral myocarditis, thyrotoxicosis, chemotherapy, excessive dietary sodium intake, and ethanol abuse

Abnormal myocardial function inhibits the ventricles from delivering adequate quantities of blood to metabolizing tissues at rest or during activity.
It results not only from a decrease in intrinsic systolic contractility of the myocardium but also from alterations in the pulmonary and peripheral circulations.
The cardiac dysfunction is either in ventricular contraction/ejection (systolic) or in ventricular filling/relaxation (diastolic).

The signs and symptoms of HF are useful in diagnosing and assessing a patient&#x27;s clinical response to therapy.
The clinical manifestations of HF are in part due to pulmonary or systemic venous congestion and edema.
When the left ventricle malfunctions, congestion initially occurs proximally in the lungs.
When the right ventricle functions inadequately, congestion in the supplying systemic venous circulation results in peripheral edema, liver congestion, and other indicators of right HF.

Class I: Patients may have symptoms of HF only at levels that would produce symptoms in normal people.
Class II: Patients may have symptoms of HF on ordinary exertion.
Class III: Patients may have symptoms of HF on less than ordinary exertion.
Class IV: Patients may have symptoms of HF at rest.

A patient with cardiac disease complains of cough and dyspnea when "walking to the mailbox." How would this patient condition be classified?
A. Class I
B. Class II
C. Class III
D. Class IV

B. Class II
Rationale: According to the NYHA, in class II cardiac disease, patients may have symptoms of HF on ordinary exertion. In class I, patient may have symptoms of HF only at levels that would produce symptoms in normal people. In class III, patient may have symptoms of HF on less than ordinary exertion, and in class IV, patients may have symptoms of HF at rest.

Stage A: Patients who are at high risk for developing HF but have no structural heart disease.
Stage B: Patients with structural heart disease who have never had symptoms of HF.
Stage C: Patients with past or current symptoms of HF associated with underlying structural heart disease.
Stage D: Patients with end-stage disease who require specialized treatment strategies, such as mechanical circulatory support, continuous IV inotrope infusions, cardiac transplantation, or hospice care.

An underlying cause of HF is treated if possible (e.g., surgical correction of structural abnormalities/valvular heart disease or medical treatment of conditions such as hypertension, diabetes mellitus, or dyslipidemia).
Precipitating factors that produce or worsen HF are identified and minimized (e.g., fever, anemia, arrhythmias, medication noncompliance, or drugs).
After these two steps, drug therapy to control the HF and improve survival becomes important.

In most cases, drug therapy is long term and consists of ACE inhibitors and beta-blockers for class I indications.
Diuretics, aldosterone antagonists, hydralazine, nitrates, digoxin (Lanoxin), and others medications are also used.
In patients with a history and reduced ejection fraction (EF), ACE inhibitors (ACE-I) or angiotensin receptor blockers (ARBs) should be used to prevent HF.
In patients with an MI and reduced EF, beta-blockers should be used to prevent HF and a statin given.

A practitioner is treating a patient post MI who has reduced EF. What would be the drug(s) of choice for this patient to prevent HF?
A. ACE inhibitor
B. ACE inhibitor and angiotensin receptor blocker
C. Beta-blocker and a statin
D. Hydralazine and a diuretic

C. Beta-blocker and a statin
Rationale: In patients with an MI and reduced EF, beta-blockers should be used to prevent HF and a statin also given. In patients with a history and reduced ejection fraction (EF), ACE inhibitors (ACEI) or angiotensin receptor blockers (ARB) should be used to prevent HF.

HF, one of the most serious consequences of cardiovascular disease, has rapidly become one of the most important health problems in cardiovascular medicine.
As the population is aging, the number of people with heart failure will significantly increase in the future.
Improved quality of life is considered a worthy health care goal, and the therapeutic approach to HF is directed toward increasing the patient's ability to maintain a positive quality of life with symptom-free activity and to enhance survival.

Tachyarrhythmia: increase in heart rate
Bradyarrhythmia: decrease in heart rate
May be asymptomatic or symptomatic
May cause palpitations, weakness, loss of consciousness, heart failure (HF), and sudden death

Myocardial ischemia; chronic HF
Hypertension; valvular heart disease
Hypoxemia
Thyroid abnormalities
Electrolyte disturbances; drug toxicity
Excessive caffeine or ethanol ingestion
Anxiety; exercise

Electrically active myocardial cells (non-pacemaker-type cells) at rest maintain a potential difference between their intracellular fluid and the extracellular fluid.
When excited, these cells manifest a characteristic sequence of transmembrane potential changes called the action potential.

Maximum diastolic depolarization
The rate of depolarization
The level of the threshold potential

Reentry involves indefinite propagation of the impulse and continued activation of previously refractory tissue.
Reentrant foci occur if there are two pathways for impulse conduction, an area of unidirectional block (prolonged refractoriness) in one of these pathways, and slow conduction in the other pathway. A refractory period occurs when the cell cannot be activated after having already fired.

Supraventricular arrhythmias: evolve above the ventricles in the atria, SA node, or AV node.
May present with either tachycardia or bradycardia or with regularity or irregularity.
AV nodal arrhythmia: originate at or within the AV node and are caused by delayed or absent SA node conduction to the AV node.
Ventricular arrhythmia: originate in the ventricles or the bundle of His; may cause loss of consciousness or death.

A patient presents with the arrhythmia torsades de pointes. What category of arrhythmia would the practitioner document?
A. Supraventricular
B. Junctional
C. Ventricular
D. Arterial

C. Ventricular
Rationale: Torsades de pointes is a rapid form of polymorphic ventricular tachycardia associated with a long QT interval.

The practitioner must first assess the patient via a thorough and sometimes urgent history and physical examination.
There may be no symptoms, or the patient may present with symptoms such as chest pain, shortness of breath, decreased level of consciousness, syncope, confusion, diaphoresis, weakness, and palpitations.
The practitioner should ask when the symptoms started, how long they have lasted, their frequency, and how the patient tolerated the symptoms.

The overall goals of AAD therapy are to relieve the acute episode of irregular rhythm, establish sinus rhythm (SR), and prevent further episodes of the arrhythmia.
Typical agents used to treat arrhythmias include AADs (classes I through IV), digoxin, adenosine, and atropine.

Class I-sodium channel blockers
Class II-beta-blockers
Class III-potassium channel blockers
Class IV-calcium channel blockers

Ia (intermediate onset/offset)
Disopyramide; procainamide; quinidine
Ib (fast onset/offset)
Lidocaine; mexiletine
Ic (slow onset/offset)
Flecainide; propafenone

Atenolol
Esmolol
Metoprolol
Propranolol

Amiodarone
Dronedarone
Sotalol
Dofetilide
Ibutilide

Diltiazem
Verapamil

Several other AADs are commonly used to treat abnormal cardiac impulse formation or conduction.
Digoxin, adenosine, and atropine are used in the treatment of various cardiac arrhythmias.

The first main question to ask when selecting drug therapy is whether the slow or fast rate of the arrhythmia makes the patient ill or symptomatic.
Second, the practitioner must think of treatable conditions that might be causing the arrhythmia.
Initial vagal maneuvers may serve as both diagnostic and therapeutic purposes for certain arrhythmias.

Atrial Fibrillation (AF) and Atrial Flutter (AFI) may be stable or unstable. Patients presenting with severe hypotension, syncope, HF, or angina would be considered to be hemodynamically unstable and would require more urgent treatment. When the patient is hemodynamically stable, the practitioner should consider conditions that may be causing the AF or AFl.

Cardiac arrhythmias are abnormal cardiac rhythms, including tachyarrhythmias (an increase in heart rate) and bradyarrhythmias (a decrease in heart rate).
Arrhythmias may be asymptomatic or symptomatic, causing palpitations, weakness, loss of consciousness, HF, and sudden death.
Searching for a reversible cause of the arrhythmia is the first step in patient care. However, many patients require chronic drug therapy for an arrhythmias that are associated with high morbidity and mortality rates.

Arcangelo, V. (2022). Pharmacotherapeutics for Advanced Practice: A Practical Approach. 5th ed.
Wolters Kluwer. Philadelphia, PA