Cardio Exam 3

Typical angina (Jin)

Results from atherosclerosis and is provoked by a variety of factors like food, exercise, and emotions

Variant (acute) angina (Jin)

Results from a sudden spasm in the coronary artery unrelated to atherosclerosis

Can occur at rest (i.e. unprovoked)

Therapy of angina (Jin)

Alleviate and prevent anginal attacks by dilating coronary artery

Three classes of antianginal drugs (Jin)

Organic nitrates

CCBs

B-adrenergic blockers

What is the class of choice to treat acute angina? (Jin)

Organic Nitrates

What are organic nitrates? (Jin)

Esters formed from simple organic alcohols with nitric acid

5 organic nitrate drugs (Jin)

Nitroglycerin

Amyl nitrite

ISDN

Pentaerythritol tetranitrate

Erythrityl Tetranitrate

Chemical nature of organic nitrates (Jin)

Volatile

The ester bond in these drugs are hydrolyzed by moisture

T/F: nitrates are effective for all types of angina (Jin)

True

How does oxygen nitrate lead to decreased preload? (Jin)

Vasodilates veins, leads to pooling of the blood in the veins, decreased venous return to the heart

How do organic nitrates lead to decreased afterload? (Jin)

Vasodilates the arteries leading to decreased resistance of peripheral tissues

MOA of organic nitrates (Jin)

Releases NO, which activates guanylate cyclase and increases cGMP levels, and reduces contractions

Dosage forms of nitrates (Jin)

Inhalation (amyl nitrite)

Injections

Tablets

Capsules

Transdermal disks

Ointments

SL nitroglycerin therapeutic effects (Jin)

Provides relief within 2 min with duration of 30 minutes

Amyl nitrite inhalation therapeutic effects (Jin)

Fast acting, onset of 15-30 seconds, lasts only 1 minute

Long acting organic nitrates (Jin)

ISDN

PETN (pentaerythritol tetranitrate)

ETN (erythrityl tetranitrate)

Long acting nitroglycerin

Adverse effects of organic nitrates (Jin)

Headache

Dizziness

N/V

Rapid pulse

Restlessness

Tolerance with long term use of nitrates

Drug interactions with organic nitrates (Jin)

Agents that cause hypotension

Sympathomimetic amines like ephedrine and norepinephrine may decrease efficacy of organic nitrates

What is an arrhythmia? (Jin)

Altered electrical impulse sequence

What part of the heart controls arrhythmias? (Jin)

Pacemaker cells in the AV and SA nodes

What causes arrhythmias? (Jin)

Pacemaker cell dysfunction

Blocks in transmission through the AV node

Atherosclerosis, hyperthyroidism, lung disease

What class of drugs are Class I antiarrhythmic drugs? (Jin)

Sodium channel blockers

What class of drugs are Class II antiarrhythmic drugs? (Jin)

B-adrenergic receptor blockers

What class of drugs are Class III antiarrhythmic drugs? (Jin)

K+ channel blockers

What class of drugs are Class IV antiarrhythmic drugs? (Jin)

Calcium channel blockers

What drug is the prototype for Class I antiarrhythmics? (Jin)

Quinidine

What drugs are in Class Ia antiarrhythmics? (Jin)

Quinidine, quinine, procainamide HCl, procaine HCl, disopyramide

Indications of quinidine (Jin)

Ventricular and supraventricular arrhythmias

Adverse effects of quinidine (Jin)

N/V, diarrhea, headache, dizziness, anti-cholinergic effects

Adverse effects of procainamide (Jin)

Drug-induced lupus syndrome, anticholinergic effects

What drugs are in Class Ib antiarrhythmics? (Jin)

Lidocaine, tocainide, mexiletine, phenytoin

Adverse effects of lidocaine (Jin)

Dizziness, paresthesia, epileptic seizures in severe cases

What drug form is lidocaine for antiarrhythmias? (Jin)

IV injection

What are the side effects of tocainide? (Jin)

GI disturbance, CNS effects

What is the main use of lidocaine? (Jin)

treatment and prevention of ventricular arrhythmias

Also drug of choice in emergency treatment

What is the main use of tocainide? (Jin)

Treatment and prevention of ventricular arrhythmias

What is the main use of mexiletine? (Jin)

Treatment and prevention of ventricular arrhythmias

Adverse effects of mexiteline (Jin)

CNS effects (similar effects to lidocaine and tocainide)

What is the main use of phenytoin? (Jin)

Treatment of atrial and ventricular arrhythmias resulting from digitalis toxicity

What is an issue with phenytoin? (Jin)

It is highly plasma bound, which means that any agent that liberates phenytoin may cause toxicity

What drugs are Class Ic antiarrhythmics? (Jin)

Flecainide, Encainide

Adverse effects of flecainide (Jin)

Can aggravate existing arrhythmias

Blurred vision, headache, headache, nausea, abdominal pain

How is encainide similar to flecainide? (Jin)

Very similar, but with less negative inotropic effect

What was the prototype of Class II Antiarrhythmic drugs (B-blockers)? (Jin)

Propranolol

MOA of class II antiarrhythmics drugs? (Jin)

Blocks effects of NE/E, decreases sympathetic activity, which decreases cAMP levels, which decreases Ca2+ influx

Also decreases conduction through AV node

Use of Class II antiarrhythmic drugs (Jin)

Treatment of supraventricular arrhythmias and digitalis-induced ventricular arrhythmias

What are the two main drugs of Class III antiarrhythmic drugs? (Jin)

Bretylium tosylate

Amiodarone

How is bretylium tosylate administered? (Jin)

Injection, only used in a hospital setting

Indication of bretylium tosylate (Jin)

The acute management of ventricular tachycardia and ventricular fibrillation

Used after 1st line treatments like defibrillation or lidocaine

Adverse effects of bretylium tosylate (Jin)

hypotension

Indication for amiodarone (Jin)

Recommended only for significant ventricular arrhythmias

Adverse effects of amiodarone (Jin)

Tired, tremor, nausea, constipation

Serious AE: lung toxicity, liver problems, heart arrhythmias, vision problems, thyroid problems

Can also cause problems in baby during both pregnancy and breastfeeding

Prototype for Class IV antiarrhythmic drugs (Jin)

Verapamil

Side effects of IV verapamil (Jin)

hypotension, bradycardia, asystole with AV block

What is CHF? (Jin)

The inability of the heart to adequately supply the body with sufficient blood flow

What is one of the most important drugs to treat CHF? (Jin)

Cardiac glycosides

Cardiac glycosides MOA (Jin)

Inhibits Na/K/ATPase pump

Drugs that interact with digoxin (Jin)

Laxatives, cholestyramine, antacids, antidiarrheal, drugs that bind plasma proteins like thyroid hormones

Signs of mild-moderate toxicity of cardiac glycosides (Jin)

Anorexia, N/V, muscular weakness, bradycardic

Signs of severe toxicity of cardiac glycosides (Jin)

Blurred vision, disorientation, diarrhea, ventricular tachycardia

Treatment of cardiac glycoside toxicity (Jin)

Discontinue drug

Administer a potassium salt

- administering K+ stimulates the Na/K/ATPase pump which decreases the intracellular Na level and decreases intracellular Ca

Positive inotropic agents (Jin)

Amrinone and milrinone

Indication of amrinone (Jin)

used in patients with severe HF refractory to other measures

Adverse effects of amrinone (Jin)

GI disturbances, thrombocytopenia, impairment of liver function

MOA of amrinone (Jin)

inhibits a phosphodiesterase, which leads to elevated cAMP, which leads to an increase in muscle contractility

Indication for milrinone (Jin)

inhibits a phosphodiesterase, which leads to elevated cAMP, which leads to an increase in muscle contractility

milrinone is a analog of amrinone

Adverse effects of milrinone (Jin)

Better tolerated than amrinone, no thrombocytopenia or GI problems

Prototype of B-adrenergic receptor agonists (Jin)

Dobutamine (IV only)

Major limitation of B-adrenergic receptor agonists (Jin)

Myocardial B-receptor desensitization

What is the leading cause of death in the US? (Jacobsen)

CVD (cardiovascular disease)

ASCVD conditions include: (Jacobsen)

CHD

Cerebrovascular disease

Peripheral artery disease

Aortic atherosclerosis

CHD includes: (Jacobsen)

Myocardial Infarction (NSTEMI or STEMI)

Coronary Artery Bypass Graft

Percutaneous Transluminal Coronary Angioplasty

Percutaneous Coronary Intervention

Stable or Unstable Angina Heart Failure

Cerebrovascular includes: (Jacobsen)

Ischemic Stroke

Transient ischemic attack (TIA)- mini stroke

Carotid artery disease

Peripheral artery disease includes: (Jacobsen)

Intermittent claudication

Critical limb ischemia

Major risk factors for ASCVD (Jacobsen)

- High LDL and Low LDL

- Smoker

- HTN

- DM

- Age (males older than 45, females older than 55)

- Obesity (BMI >30)

-Physical inactivity

- Diet high in saturated fats

Modifiable risk factors for ASCVD (Jacobsen)

High cholesterol

HTN

Smoking

Obesity

Diabetes

Nutrition, diet, inactivity

What is primary prevention of ASCVD? (Jacobsen)

Prevent initial development of ASCVD

What is secondary prevention of ASCVD? (Jacobsen)

Prevent further progression or death from ASCVD

Adding medications like aspirin, cholesterol medications, and diabetes therapy is most favorable in this population

When should risk assessment for ASCVD begin? (Jacobsen)

At a young age- elevated risk factor levels are detectable in adolescents and young adults

Higher risk= greater benefit of preventative measures

Lifestyle management to reduce ASCVD risk (Jacobsen)

Diet- rich in vegetables, fruits, whole grains, low fat dairy; limit sodium, sweets, trans fats, red meats, saturated fats

Physical activity- 2 h 30 min, moderate-intensity

Healthy weight

ABCDs of ASCVD (Jacobsen)

A- Aspirin, for select patients only

B- Blood pressure, achieve treatment goals in patients with HTN

C- Cholesterol, statin therapy in patients

D- Diabetes, Metformin, SGLT-2 inhibitors, or GLP-1 agonists

S- Smoking cessation

Net ASCVD benefit increases as the absolute risk ___________. (Jacobsen)

Increases

What were the results of the ARRIVE trial? (Jacobsen)

There was no difference between aspirin and the placebo

GI bleed rates were higher with aspirin

What were the results of the ASPREE trial? (Jacobsen)

There was no difference in CVD between aspirin and placebo

Risk of major hemorrhages higher with aspirin

What were the results of the ASCEND trial? (Jacobsen)

There were lower rates of efficacy with aspirin compared to placebo

Higher rates of AEs with aspirin

How many US adults have some form of CVD? (Jacobsen)

1 in 3

What causes stable ischemic heart disease? (Jacobsen)

Caused by an obstructive atherosclerotic plaque in coronary vessel(s)

What is the main symptom of myocardial ischemia in patients with SIHD? (Jacobsen)

Chest pain (angina pectoris)

Is initial manifestation in ~50% of patients

Causes of increased O2 demand (Jacobsen)

tachycardia

HTN

anxiety

left ventricular hypertrophy

aortic stenosis

hyperthyroidism

cocaine, meth

Causes of O2 supply (Jacobsen)

atherosclerosis

pulmonary hypoxemia

anemia

left ventricular dysfunction

aortic stenosis

cocaine

Clinical characteristics of angina (Jacobsen)

Pain (heavy, crushing, suffocating)

generally lasts a few minutes

does not change with respiration or position

most often due to CAD-related ischemia

Only evidence of myocardial ischemia (Jacobsen)

ECG of evidence (some patients may have silent ischemia)

ST segment depression is a sign of myocardial ischemia

Testing methods for myocardial ischemia and CAD (Jacobsen)

ECG

Stress Test

Cardiac CT or MRI

Coronary angiogram or cardiac catheterization

Types of SIHD (Jacobsen)

Stable exertional angina- most common

Variant Angina- at rest and in younger patients

Silent myocardial ischemia

Goals of treatment of SIHD (Jacobsen)

Decrease morbidity and mortality

eliminate chest pain and return to normal activities

Importance of shared decision making (Jacobsen)

The patient remains involved in key decisions, this is high quality care

Substance abuse and CCD (Jacobsen)

Alcohol

Cocaine, meth- stimulate SNS, platelet aggregation, increased O2 demand

Opioids

Marijuana- stimulate SNS, platelet activation, endothelial dysfunction

GDMT in CCD (Jacobsen)

Lipid management: lifestyle changes, moderate or high-intensity statin

Blood pressure management: lifestyles changes,

Antiplatelet therapy in CCD (Jacobsen)

Aspirin 81 mg continued indefinitely unless contraindicated

Clopidogrel 75 mg is a reasonable alternative if aspirin is contraindicated

MOA of aspirin (Jacobsen)

Irreversibly blocks COX in platelets, which decreases clot formation