Cardio

ANATOMY AND PHYSIOLOGY OF THE HEART

The heart is a hollow, muscular organ located in the center of the thorax, where it occupies the space between the lungs (mediastinum) and rests on the diaphragm. It weighs approximately 300 g (10.6 oz);

THREE LAYERS OF THE HEART

  • ENDOCARDIUM (Inner Layer)

  • MYOCARDIUM (Middle Layer)

  • EPICARDIUM (Exterior Layer)

  • • The space between these two layers (pericardial space) is filled with about 30 mL of fluid, which lubricates the surface of the heart and reduces friction during systole.

HEART CHAMBERS

Pumping includes relaxation and contraction of the muscular walls of its two top chambers (atria) and two bottom chambers (ventricles).

THE RIGHT SIDE OF THE HEART

  • Made up of the right atrium and right ventricle distributes venous blood (deoxygenated blood) to the lungs via the pulmonary artery (pulmonary circulation) for oxygenation.

  • The right atrium receives blood returning from the superior vena cava (head, neck, and upper extremities), inferior vena cava (trunk and lower extremities), and coronary sinus (coronary circulation).

THE LEFT SIDE OF THE HEART

  • Is the left atrium and left ventricle, distributes oxygenated blood to the remainder of the body via the aorta (systemic circulation).

  • The left atrium receives oxygenated blood from the pulmonary circulation via the pulmonary veins.

HEART CHAMBERS

Diastole (relaxation phase)

  • Referred to as the period of ventricular filling

Systole

  • Events of contraction of the atria and the ventricles

  • Not simultaneous

TYPES OF HEART VALVES

ATRIOVENTRICULAR VALVES - separate the atria from the valves

  • Tricuspid Valve - separates the right atrium from right ventricle

  • Mitral or Bicuspid Valve - Lies between the left atrium and left ventricle

SEMILUNAR VALVES - Composed of three leaflets that are moon-shaped

  • Pulmonic Valve - the valve between the right ventricle and the pulmonary artery

  • Aortic Valve - the valve between the left ventricle and the aorta

  • Closed during diastole

DRUGS THAT AFFECT THE CARDIOVASCULAR SYSTEM

ACE INHIBITORS

Therapeutic Actions and Indications

  • Act in the lungs to prevent ACE from converting angiotensin I to angiotensin Il, a powerful vasoconstrictor and stimulator of aldosterone release.

  • This action leads to a decrease in blood pressure and in aldosterone secretion, with a resultant slight increase in serum potassium and a loss of serum sodium and fluid.

Contraindications and Cautions

  • ACE inhibitors are contraindicated in the presence of allergy to any of the ACE inhibitors to prevent hypersensitivity reactions and with impaired renal function, which could be exacerbated by the effects of this drug in decreasing renal blood

  • Caution should be used in patients with heart failure because the change in hemodynamics could be detrimental in some cases and in those with salt/volume depletion, which could be exacerbated by the drug effects.

Adverse Effects

• reflex tachycardia

• chest pain

• Angina

• heart failure

• cardiac arrhythmias; gastrointestinal (Gl) irritation, ulcers, constipation, and liver injury; renal insufficiency, renal failure, and proteinuria; and rash, alopecia, dermatitis, and photosensitivity

ANGIOTENSIN II RECEPTOR BLOCKERS

Therapeutic Actions and Indications

• The ARBs selectively bind with the angiotensin Il receptors in vascular smooth muscle and in the adrenal cortex to block vasoconstriction and the release of aldosterone. These actions block the blood pressure-raising effects of the renin-angiotensin system and lower blood pressure

Adverse Effects

The adverse effects most commonly associated with ARBs include the following:

  • headache, dizziness

  • syncope, weakness

  • Hypotension

  • GI complaints, including diarrhea, abdominal pain, nausea, dry mouth, and tooth pain

  • symptoms of upper respiratory tract infections, cough

  • rash, dry skin, and alopecia

CALCIUM CHANNEL BLOCKERS

  • Calcium channel blockers decrease blood pressure, cardiac workload, and myocardial oxygen consumption.

  • The effects of these drugs on cardiac workload also make them very effective in the treatment of angina

Therapeutic Actions and Indications

  • Calcium channel blockers inhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells, altering the action potential and blocking muscle cell contraction.

  • This effect depresses myocardial contractility, slows cardiac impulse formation in the conductive tissues, and relaxes and dilates arteries, causing a fall in blood pressure and a decrease in venous return.

Contraindications and Cautions

  • Presence of allergy - to prevent hypersensitivity reactions

  • With heart block or sick sinus syndrome- could be exacerbated by the conduction-slowing effects of these drugs

  • With renal or hepatic dysfunction- could alter the metabolism and excretion of these drugs

Adverse Effects

• The adverse effects associated with these drugs relate to their effects on cardiac output and on smooth muscle.

CNS

  • Dizziness

  • light-headedness

  • Headache

  • fatigue.

GI

  • nausea and hepatic injury

CVS

  • Hypotension

  • Bradycardia

  • peripheral edema

  • heart block

  • Skin flushing and rash

VASODILATORS

The vasodilators are reserved for use in severe hypertension or hypertensive emergencies.

Therapeutic Actions and Indications

  • The vasodilators act directly on vascular smooth muscle to cause muscle relaxation, leading to vasodilation and drop in blood pressure. They do not block the reflex tachycardia that occurs when blood pressure drops

Adverse Effects

  • Dizziness

  • Anxiety

  • Headache

  • Reflex tachycardia

  • Heart failure

  • Chest pain

  • Edema

  • Skin rash and lesions

  • Gl upset, nausea, and vomiting

Cyanide toxicity :

  • Dyspnea, headache

  • Vomiting, dizziness

  • Ataxia, loss of consciousness

  • Imperceptible pulse, absent reflexes

  • Dilated pupils, pink color, distant heart sounds, and shallow breathing

Diuretic Agents

  • are drugs that increase the excretion of sodium and water from the kidney

  • Diuretics are very important for the treatment of hypertension. These drugs are often the first agents tried in mild hypertension; they affect blood sodium levels and blood volume.

Loop Diuretics

  • They inhibit the sodium and chloride reabsorption in the thick segment of the ascending limb of the loop of Henle as well as in the proximal convoluted tubule and the distal diluting site

Thiazide Diuretics

  • Inhibit sodium and chloride reabsorption in the distal convoluted tubule

  • These drugs are the first-line drugs used to manage essential hypertension when drug therapy is needed

Potassium Sparing Diuretics

  • The potassium-sparing diuretics are not as powerful as the loop diuretics, but they retain potassium instead of wasting it

Contraindications

  • Hypersensitivity

  • Fluid and electrolyte imbalances

  • Severe renal failure

Cautious administration with

  • Systemic lupus erythematous ( SLE)

  • Gout

  • Pregnancy and lactation

Side Effects

  • Common side effects

  • Gl upset

  • fluid and electrolyte imbalances

  • hypotension

  • electrolyte disturbances

Side effects (thiazide and loop diuretics)

  1. Hypokalemia weakness, muscle cramps, and arrhythmia

  2. Hypercalcemia

  3. Decreased excretion of uric acid

Renin Inhibitor

  • Aliskiren directly inhibits renin, leading to decreased plasma renin activity and inhibiting the conversion of angiotensinogen to angiotensin I.

  • This inhibition of the renin-angiotensin-aldosterone system leads to decreased blood pressure, decreased aldosterone release, and decreased sodium reabsorption.

Sympathetic Nervous System Blockers

  1. Drugs that block the effects of the sympathetic nervous system are useful in blocking many of the compensatory effects of the sympathetic nervous

    1. Beta-blockers - block vasoconstriction, decrease heart rate, decrease cardiac muscle contraction, and tend to increase blood flow to the kidneys, leading to a decrease in the release of renin.

    2. Alpha- and beta-blockers- are useful in conjunction with other agents and tend to be somewhat more powerful, blocking all of the receptors in the sympathetic system.

    3. Alpha-adrenergic blocker - inhibit the postsynaptic alpha1-adrenergic receptors, decreasing sympathetic tone in the vasculature and causing vasodilation, which leads to a lowering of blood pressure.

    4. Alphal-blockers - are used to treat hypertension because of their ability to block the postsynaptic alphal-receptor sites. This decreases vascular tone and promotes vasodilation, leading to a fall in blood pressure.

    5. Alpha2-agonists - stimulate the alpha2receptors in the CNS and inhibit the cardiovascular centers, leading to a decrease in sympathetic outflow from the CNS and a resultant drop in blood pressure.

ANTIHYPOTENSIVE AGENTS

• if blood pressure becomes too low (hypotension), the vital centers in the brain and the rest of the tissues of the body may not receive suffi cient oxygenated blood to continue functioning

ANTIHYPOTENSIVE AGENTS

SYMPATHETIC ADRENERGIC AGONISTS OR VASOPRESSORS

  • Sympathomimetic drugs are the first choice for treating severe hypotension or shock.

Adverse Effects

  • Decreased GI activity with nausea and constipation

  • Increased respiratory

  • Changes in blood pressure

  • Headache

  • Changes in peripheral blood flow with numbness, tingling,

  • Tachycardia

  • Hypertension

ALPHA-SPECIFIC ADRENERGIC AGENTS

  • • Midodrine (ProAmatine) is an alpha-specific adrenergic agent used to treat orthostatic hypotension— hypotension that occurs with position change—that interferes with a person's ability to function and has not responded to any other therapy.

  • Cardiotonic agents are drugs used to increase the contractility and output in a hypodynamic heart without propotionate increase in 02 consumption

  • Commonly used in the treatment of heart failure (HF)

  • Cardiotonic (inotropic) drugs affect the intracellular calcium levels in the heart muscle, leading to increased contractility.

  • This increase in contraction strength leads to increased cardiac output, which causes increased renal blood flow and increased urine production

CARDIAC GLYCOSIDES

  • Digoxin (Lanoxin) commonly used drug

  • The cardiac glycosides were originally derived from Digitalis purpurea (Common Foxglove)

Mechanism of action

Digoxin increases intracellular calcium and allows more calcium to enter myocardial cells during depolarization.

That results:

  1. Increased force of myocardial contraction (a positive inotropic effect)

  2. Increased cardiac output and renal perfusion

  3. Slowed heart rate, owing to slowing of the rate of cellular repolarization (a negative chronotropic effect)

  4. Decreased conduction velocity through the atrioventricular AV) node

INDICATIONS

  • Heart failure (HF)

  • Atrial flutter

  • Atrial fibrillation

  • Paroxysmal atrial tachycardia

Contraindications

  • Hypersensitivity to digitalis preparations

  • Ventricular tachycardia or fibrillation

  • Heart block or sick sinus syndrome

  • Idiopathic hypertrophic subaortic stenosis (IHSS)

  • Acute MI

  • Renal failure

Adverse Effects

  • Headache, weakness, drowsiness and vision changes

  • Digitalis toxicity ( serious side effect)

Digitalis toxicity

  • A serious syndrome that can occur when digoxin levels are too high

  • Normal level- 0.5 -2.0 ng/ml signs and symptoms - anorexia, nausea, vomiting, malaise, depression, irregular heart rhythms including heart block, atrial arrhythmias, and ventricular tachycardia

  • Antidote- Digoxin immune Fab (DigiFab)

Nurses responsibilities

  • Assess for contraindications or cautions

  • Perform a physical assessment

  • Assess cardiac status closely, including pulse and blood pressure

  • Monitor apical pulse for 1 full minute before administering the drug

  • Hold the dose if the pulse is less than 60 beats min in an adult or less than 90 beats min in an infant; retake the pulse in 1 hour. If the pulse remains low, document it, withhold the drug, and notify the prescriber

  • Monitor the pulse for any change in quality or rhythm

  • Administer intravenous doses very slowly over at least 5 minutes to avoid cardiac arrhythmias and adverse effects.

  • Avoid administering the oral drug with food or antacids to avoid delays in absorption

  • Obtain digoxin level as ordered; monitor the patient for therapeutic digoxin level (0.5-2 ng/mL)

  • Maintain emergency equipment on standby if digoxin toxicity develops

  • Provide thorough patient teaching, including the name of the drug, dosage prescribed, technique for monitoring pulse and acceptable pulse parameters, dietary measures if appropriate, measures to avoid adverse effects, warning signs of possible toxicity and need to notify health care provider

PHOSPHODIESTERASE INHIBITORS

Milrinone (Primacor)

  • This drugs block the enzyme phosphodiesterase. This blocking effect leads to an increase in myocardial cell cyclic adenosine monophosphate (cAMP), which increases calcium levels in the cell

INDICATIONS

  • Short-term treatment of HF that has not responded to digoxin or diuretics alone or that has had a poor response to digoxin, diuretics, and vasodilators

Contraindications

  • Hypersensitivity to phosphodiesterase inhibitors

  • Severe aortic or pulmonic valvular disease

  • Acute MI

Adverse Effects

  • ventricular arrhythmias (which can progress to fatal ventricular fibrillation), hypotension, and chest pain

  • Gl effects include nausea, vomiting, anorexia, and abdominal pain

  • Thrombocytopenia occurs frequently with milrinone

  • Precipitates form when these drugs are given in solution with furosemide

Nurses Responsibilities

  • Assess for contraindications or cautions: any known allergies to these drugs or to avoid hypersensitivity reactions;

  • acute aortic or pulmonic valvular disease,

  • acute myocardial infarction

  • ventricular arrhythmias

  • Pregnancy and lactation

  • Assess cardiac status closely, including pulse and blood pressure

  • Protect the drug from light to prevent drug degradation

  • Monitor input and output and record daily weight

  • Monitor platelet counts before and regularly during therapy to ensure that the dose is appropriate, inspect the skin for bruising or petechiae to detect early signs of thrombocytopenia

  • Provide life-support equipment on standby

  • Provide thorough patient teaching, including the name of the drug, dosage prescribed, measures to avoid adverse effects, warning signs of problems, and the need for periodic monitoring and evaluation

ANGINA

  • It is a pain syndrome due to induction of an adverse oxygen supply/demand situation in a portion of myocardium

Antianginal drugs are used to help restore the appropriate supply-and-demand ratio in oxygen delivery to the myocardium.

Indication for :

1. CORONARY ARTERY DISEASE (CAD)

• The narrowing of the vessels is caused by the development of atheromas, or fatty tumors in the intima of the vessels, in a process called atherosclerosis

2. ACUTE MYOCARDIAL INFARCTION

• A coronary vessel becomes completely occluded and is unable to deliver blood to the cardiac muscle, the area of muscle that depends on that vessel for oxygen becomes ischemic and then necrotic.

How they act

• These drugs can work to improve blood delivery to the heart muscle

  1. by dilating blood vessels (i.e., increasing the supply of oxygen)

  2. by decreasing the work of the heart (i.e.decreasing the demand for oxygen).

Classification

Nitrates

  • Nitrates are drugs that act directly on smooth muscle to cause relaxation and to depress muscle tone

Mechanism of action

  • The nitrates relax and dilate veins, arteries, and capillaries, allowing increased blood flow through the vessels and lowering systemic blood pressure because of a drop in resistance.

  • Nitrates decreases the preload and afterload

INDICATIONS

  • LONG ACTING NITRATES

    • Taken before chest pain begins in situations in which exertion or stress can be anticipated for prevention of angina in adults; taken daily for management of chronic angina

  • SHORT ACTING NITRATES

    • Treatment of acute angina attack; prevention of anginal attacks

Contraindications

  • Hypersensitivity

  • Severe anemia

  • Head trauma or cerebral hemorrhage

  • pregnancy or lactation

Adverse effect

Central nervous system (CNS)

  • Headache

  • Dizziness

  • weakness

Gastrointestinal (GI)

  • nausea, vomiting

  • Incontinence

Cardiovascular

  • Hypotension

Integumentary

  • Flushing

  • Pallor

  • increased perspiration

Nurses responsibilities

  • Assess for contraindications

  • Assess cardiopulmonary status closely, including pulse rate, blood pressure, heart rate, and rhythm (30min)

  • Always check the expiration date on the bottle and protect the medication from heat and light.

  • Instruct the patient that a sublingual dose may be repeated in 5 minutes if relief is not felt, for a total of three doses; if pain persists, the patient should go to an emergency room

  • Rotate the sites of topical form

  • Taper the dose gradually (over 4 to 6 weeks) after long-term therapy

BETA BLOCKERS

  • Beta-adrenergic blockers are used to block the stimulatory effects of the sympathetic nervous system.

Mechanism of action

  • The beta-blockers competitively block beta-adrenergic receptors in the heart and decreasing the influence of the SNS on these tissues. The result is a decrease in the excitability of the heart, a decrease in cardiac output, a decrease in cardiac oxygen consumption, and a lowering of blood pressure.

INDICATIONS

  • Long-term management of angina pectoris.

  • To prevent reinfarction in stable patients 1 to 4 weeks after an MI

CONTRAINDICATIONS

  • Bradycardia, heart block, and cardiogenic
    shock

  • Pregnancy and lactation

  • Cautious administration to Asthma, chronic obstructive pulmonary disease, or thyrotoxicosis

NURSES RESPONSIBILITIES

  • Assess for contraindications or cautions

  • Do not stop these drugs abruptly after chronic therapy, but taper gradually over 2 weeks

  • Monitor blood pressure, pulse, rhythm, and cardiac output regularly

  • Continuously monitor any patient receiving an intravenous form of these drugs

CALCIUM CHANNEL BLOCKERS

MECHANISM OF ACTION

  • Calcium channel blockers inhibit the movement of calcium ions across the membranes of myocardial and arterial muscle cells, altering the action potential and blocking muscle cell

  • This will results loss of smooth muscle tone, vasodilation, and decreased peripheral resistance occur

INDICATIONS

Treatment of :

  • Prinzmetal angina

  • Chronic angina

  • Effort associated angina

  • Hypertension.

  • Verapamil is also used to treat cardiac tachyarrhythmias because it slows conduction more than the other calcium channel blockers do

Contraindications

  • Hypersensitivity

  • Pregnancy and lactation

Caution should be used with

  • Heart block or sick sinus syndrome

  • Renal or hepatic dysfunction

  • Heart Failure

Adverse Effects

  • CNS -dizziness, light-headedness, headache, and fatigue.

  • GI- nausea and hepatic injury related to direct toxic effects on hepatic cells.

  • Cardiovascular -hypotension, bradycardia, peripheral edema, and heart block.

  • Skin- flushing and rash

NURSES RESPONSIBILITIES

  • Assess for contraindications

  • Inspect skin for color and integrity

  • Monitor blood pressure very carefully

  • Provide thorough patient teaching

Potassium channel openers

  • Potassium channel openers activates the ATP sensitive potassium channels thereby hyperpolarising the vascular smooth muscles.

  • This results in reduction in vascular tone

  • That will lead to a decrease in preload and afterload

  • EG- Nicorandil

INDICATIONS

  • Prevention and long term treatment of chronic stable angina pectoris

  • Reduction in the risk of acute coronary syndromes in patients with chronic stable angina

Contraindications

  • Hypersensitivity

  • Cardiogenic shock

  • hypotension

Side effects

  • Flushing

  • Palpitation

  • Weakness

  • Headache

  • Dizziness

  • vomiting

Nurses Responsibilities

  • Assess the hypersensitivity and contraindications

  • Regular monitoring of vital signs

  • Health education

  • asses the oral cavity for oral ulcers

OTHERS- IVABRADINE

  • Ivabradine is a newer type of drug

Mechnism of action

  • it acts by reducing the heart rate by specific inhibition of the funny channel (cyclic nucleotide-gated)

  • It specifically inhibits the cardiac pacemaker and therby reducing heart rate

Indications

  • Chronic stable angina patients with normal sinus rhythm

  • Chronic heart failure

Contraindications

  • Resting heart rate less than 70

  • Cardiogenic shock

  • Acute MI

  • Sick sinus syndrome

  • Severe hepatic injury

  • Pregnancy and lactation

Side effects

  • Blurred vision

  • Bradycardia

  • Syncope

  • Headache

  • Constipation

  • Muscle cramps

Nurses Responsibilities

  • Check for hypersensitivity and contraindications

  • Assess the pulse rate and blood pressure

  • Check the liver function test regularly

  • Check for visual disturbances

  • Health education

Antiarrhythmic Agents

Arrhythmias

  • involve changes to the automaticity or conductivity of the heart cells.

  • Affect the action potential of the cardiac cells by altering their automaticity, conductivity, or both.

  • The cardiac conduction system determines the heart's rate and rhythm. The property by which the cardiac cells generate an action potential internally to stimulate the cardiac muscle without other stimulation is known as automaticity.

Arrhythmias can be caused by changes in rate:

  • Tachycardia

  • Bradycardia

  • Premature atrial contractions (PACs)

  • Premature ventricular contractions (PVCs)

Classes of Antiarrhythmias Drugs

  • CLASS I ANTIARRHYTHMICS-are drugs that block the sodium channels in the cell membrane during an action potential

  • CLASS II ANTIARRHYTHMICS- are beta-adrenergic blockers that block beta-receptors, causing a depression of phase 4 of the action potential

  • CLASS III ANTIARRHYTHMICS- block potassium channels and slow the outward movement of potassium during phase 3 of the action potential, prolonging it

  • CLASS IV ANTIARRHYTHMICS- block the movement of calcium ions across the cell membrane, depressing the generation of action potentials and delaying phases 1 and 2 of repolarization, which slows automaticity and conduction

  • OTHER ANTIARRHYTHMICS- Adenosine is another antiarrhythmic agent that is used to convert supraventricular tachycardia to sinus rhythm if vagal maneuvers have been ineffective.

Adverse Effects

  • Central nervous system (CNS)

  • dizziness, drowsiness

  • Fatigue,twitching

  • mouth numbness, slurred speech

  • vision changes, and tremors that can progress to convulsions.

GI

  • changes in taste, nausea, and vomiting.

Cardiovascular effects include the proarrhythmic effects:

  • arrhythmias (including heart blocks)

  • hypotension, vasodilation

  • and the potential for cardiac arrest

  • Respiratory depression

Lowering-Lipid Agents

  • This is to lower serum levels of cholesterol and various lipias.

  • These drugs are sometimes called antihyperlipidemic agents used to treat hyperlipidemia-an increase in the level of lipids in the blood.

Fats and Biotransformation (Metabolism)

  • The presence of these products in the duodenum stimulates contraction of the gallbladder and the release of bile.

  • Bile acids, which contain high levels of cholesterol (a fat), act like a detergent in the small intestine and break up the fats into small units, called micelles, which can be absorbed into the wall of the small intestine.

Lipoproteins

  • The lipoproteins produced in the liver that have well known clinical implications are the low-density lipoproteins (LDLs) and the high-density lipoproteins (HDLs).

Cholesterol

  • The body needs fats, particularly cholesterol, to maintain normal function. choless us descally provided through the diet and the fat metabolism

  • Every cell in the body has the metabolic capability of producing cholesterol. The enzyme hydroxymethylglutaryl-coenzyme A (HMG-CoA) reductase regulates the early, rate-limiting step in the cellular synthesis of cholesterol.

Hyperlipidemias

  • When the levels of lipids in the blood increase, hyperlipidemia occurs.

  • This can result from excessive dietary intake of fats or from genetic alterations in fat metabolism leading to a variety of elevated fats in the blood:

    • Hypercholesterolemia

    • Hypertriglyceridemia

    • alterations in LDL and HDL concentrations

BILE ACID SEQUESTRANTS

  • Bile acid sequestrants are used to decrease plasma cholesterol levels.

  • Three bile acid sequestrants currently in use are:

  1. cholestyramine (Questran

  2. colestipol (Colestid)

  3. colesevelam (WelChol)

Therapeutic Actions and Indications

  • Bile acid sequestrants bind with bile acids in the intestine to form an insoluble complex that is then excreted in the feces.

  • Bile acids contain high levels of cholesterol. As a result, the liver must use cholesterol to make more bile acids.

Contraindications and Cautions

Bile acid sequestrants are contraindicated :

  • in the presence of allergy to any bile acid

  • complete biliary obstruction

  • abnormal intestinal function

  • pregnancy or lactation

Therapeutic Actions and Indication

  • The early rate-limiting step in the synthesis of cellular cholesterol involves the enzyme HMG-CoA reductase. If this enzyme is blocked, serum cholesterol and LDL levels decrease because more LDLs are absorbed by the cells for processing into cholesterol.

Cholesterol Absorption Inhibitors

Therapeutic Actions and Indications

  • Ezetimibe works in the brush border of the small intestine to decrease the absorption of dietary cholesterol from the small intestine. As a result, less dietary cholesterol is delivered to the liver, and the liver increases the clearance of cholesterol from the serum to make up for the drop in dietary cholesterol, causing the total serum cholesterol level to drop

Adverse Effects

The most common adverse effects associated with ezetimibe are:

  • Mild abdominal pain

  • Diarrhea

  • Bloating and flatulence

  • Headache

  • Dizziness

  • Fatigue

  • Upper respiratory tract infection (URI)

  • Back pain

  • Muscle aches and pains

Other Lipid-lowering Agents

Fibrates

  • The fi brates stimulate the breakdown of lipoproteins from the tissues and their removal from the plasma. They lead to a decrease in lipoprotein and triglyceride synthesis and secretion.

  • Vitamin B Vitamin B3, known as niacin (Niaspan) or nicotinic acid, inhibits the release of free fatty acids from adipose tissue, increases the rate of triglyceride removal from plasma, and generally reduces LDL and triglyceride levels and increases HDL levels.

Future Therapies

  • The endocannabinoids are substances present in the body that activate various neurological receptors that seem to be very important in the body's regulation of appetite, satiety, and lipid metabolism. With blocking of the endocannabinoid system, a series of changes occur that would seem to have a very profound effect on many components of the metabolic syndrome.