7  Perfusion:    Hypertension and Antihypertensives, Hyperlipidemia and Antihyperlipidemic

In the intricate system of cardiovascular health, the relationship between perfusion, hypertension, and dyslipidemia is deeply intertwined, each influencing the others in complex ways. Perfusion, the process of delivering oxygenated blood to tissues throughout the body, is critically dependent on maintaining optimal blood pressure and lipid levels. Hypertension, or elevated blood pressure, disrupts this balance, leading to increased strain on the heart and blood vessels, which can ultimately impair perfusion and contribute to the development of cardiovascular diseases. Similarly, dyslipidemia, characterized by abnormal levels of lipids in the blood, exacerbates this risk by promoting atherosclerosis. In this condition, fatty deposits build up in the arteries, further impeding blood flow and elevating blood pressure.

This chapter will explore the intricate connections between these conditions, beginning with understanding the etiology, pathophysiology, and clinical manifestations of blood pressure control. We will discuss non-pharmacological measures to manage hypertension, emphasizing lifestyle modifications that can profoundly impact reducing cardiovascular risk. The chapter will then delve into the pharmacological management of hypertension, providing a comprehensive overview of various drug classes, including adrenergic blocking agents, ACE inhibitors, calcium channel blockers, and antilipemic. Each medication’s mechanism of action, indications for use, adverse effects, and implications for nursing practice will be thoroughly examined. This chapter draws from knowledge of normal mechanisms of perfusion learned in the previous chapter.

Additionally, we will explore the etiology, pathophysiology, and clinical manifestations of dyslipidemia, along with non-pharmacologic strategies and interventions to enhance therapeutic outcomes. The chapter will also cover the use of antilipemic agents, detailing their mechanisms, indications, and nursing considerations. Finally, we will discuss the rationale behind medication combinations to control hypertension and manage dyslipidemia effectively, highlighting the importance of a holistic approach to cardiovascular care. By understanding these interconnected pathways, you will be better equipped to manage and educate patients on preventing and treating hypertension and dyslipidemia, ultimately improving their cardiovascular health and overall well-being.

I. Circulation, Perfusion, and Blood Pressure Defined 

“Circulation is the continuous movement of blood throughout the body, driven by the pumping action of the heart.”

Systematic Circulation: Blood Vessels:

After blood is pumped out of the ventricles, it is carried through the body via blood vessels. An artery is a blood vessel that carries blood away from the heart, where it branches into ever-smaller vessels and eventually into tiny capillaries where nutrients and wastes are exchanged at the cellular level. Capillaries then combine with other small blood vessels that carry blood to a vein, a larger blood vessel that returns blood to the heart. Compared to arteries, veins are thin-walled, low-pressure vessels. Larger veins are also equipped with valves that promote the unidirectional flow of blood toward the heart and prevent backflow caused by the inherent low blood pressure in veins as well as the pull of gravity.

In addition to their primary function of returning blood to the heart, veins may be considered blood reservoirs because systemic veins contain approximately 64 percent of the blood volume at any given time. Approximately 21 percent of the venous blood is located in venous networks within the liver, bone marrow, and integument. This volume of blood is referred to as venous reserve. Through vasoconstriction, this reserve volume of blood can get back to the heart more quickly for redistribution to other parts of the circulation.

Perfusion is the ability of the heart to move oxygen and nutrients throughout the body via the circulatory or lymphatic systems to the capillaries to ensure cellular processes function appropriately.  Perfusion is cyclical, meaning that to provide oxygen and nutrients to the cell, the body must also be able to remove cellular wastes and by-products. Inadequate perfusion, also called ischemia, may be the cause of several cardiovascular diseases, including cardiovascular disease, coronary artery disease, cerebrovascular disease, peripheral artery disease, and many other conditions.

Blood Pressure 

A blood pressure reading is the measurement of the force of blood against the walls of the arteries as the heart pumps blood through the body. It is reported in millimeters of mercury (mmHg). This pressure changes in the arteries when the heart is contracting compared to when it is resting and filling with blood.

The systolic blood pressure is the maximum pressure on the arteries during systole, the phase of the heartbeat when the ventricles contract (beating). This is the top number of blood pressure readings. Systole causes the ejection of blood out of the ventricles and into the aorta and pulmonary arteries. The diastolic blood pressure is the resting pressure on the arteries during diastole, the phase between each contraction of the heart when the ventricles are filling with blood. This is the bottom number of the blood pressure reading. Therefore, 120/80 indicates the systolic blood pressure is 120 mm Hg, and the diastolic blood pressure is 80 mm Hg.

Many factors can affect blood pressure, such as hormones, stress, exercise, eating, caffeine, heavy alcohol consumption, sitting, and standing. Blood flow through the body is regulated by the size of blood vessels, the action of smooth muscle, one-way valves, and the fluid pressure of the blood itself. Blood Flow and Blood Pressure Regulation.

II. Physiology  of Blood Pressure and Pathophysiology of Hypertension

Blood Pressure

Any factor that causes cardiac output to increase, by elevating heart rate or stroke volume or both, will elevate blood pressure and promote blood flow. These factors include sympathetic stimulation, the catecholamines epinephrine and norepinephrine, thyroid hormones, and increased calcium ion levels. Conversely, any factor that decreases cardiac output, by decreasing heart rate, stroke volume, or both, will decrease arterial pressure and blood flow. These factors include parasympathetic stimulation, elevated or decreased potassium ion levels, decreased calcium levels, anoxia, and acidosis. Blood pressure increases with increased cardiac output, peripheral vascular resistance, blood volume, blood viscosity, and rigidity of vessel walls. Blood pressure decreases with decreased cardiac output, peripheral vascular resistance, blood volume, blood viscosity, and vessel wall elasticity.

Blood pressure is influenced by:

• Heart rate (HR) can vary considerably, not only with exercise and fitness levels but also with age. Newborn resting HRs may be 120 -160 bpm. HR gradually decreases until young adulthood and then gradually increases again with age. For an adult, normal resting HR will be in the range of 60–100 bpm. Bradycardia is the condition in which the resting rate drops below 60 bpm, and tachycardia is the condition in which the resting rate is above 100 bpm.
• Stroke volume (SV) is the amount of blood in one clean pump – in other words, what your heart pumps with each beat. It measures how much blood goes through your body every minute. Results depend on the size of the heart and how fast it contracts. Stroke volume (SV) is also used to calculate ejection fraction, the portion of the blood pumped or ejected from the heart with each contraction. Many of the same factors that regulate HR also impact cardiac function by altering SV. Three primary factors affecting stroke volume are preload or the stretch on the ventricles before contraction; contractility, or the force or strength of the contraction itself; and afterload, the force the ventricles must generate to pump blood against the vessel’s resistance. Many cardiovascular medications affect cardiac output by affecting preload, contractility, or afterload.
• Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle in one minute. To calculate this value, multiply stroke volume (SV), the amount of blood pumped by each ventricle, by the heart rate (HR) in beats per minute. It can be represented mathematically by the following equation: CO = HR × SV. Factors influencing CO include autonomic innervation by the sympathetic and parasympathetic nervous system and hormones such as epinephrine, preload, contractility, and afterload. SV is also used to calculate ejection fraction, the portion of the blood pumped or ejected from the heart with each contraction.

Any factor that causes cardiac output to increase, by elevating heart rate or stroke volume or both, will elevate blood pressure and promote blood flow. These factors include sympathetic stimulation, the catecholamines epinephrine and norepinephrine, thyroid hormones, and increased calcium ion levels. Conversely, any factor that decreases cardiac output, by decreasing heart rate, stroke volume, or both, will decrease arterial pressure and blood flow. These factors include parasympathetic stimulation, elevated or decreased potassium ion levels, decreased calcium levels, anoxia, and acidosis.

• Peripheral vascular resistance refers to compliance, which is the ability of any compartment to expand to accommodate increased content. A metal pipe, for example, is not compliant, whereas a balloon is. The greater the compliance of an artery, the more effectively it is able to expand to accommodate surges in blood flow without increased resistance or blood pressure. Veins are more compliant than arteries and can expand to hold more blood. When vascular disease causes stiffening of arteries (e.g., atherosclerosis or arteriosclerosis), compliance is reduced, and resistance to blood flow is increased. The result is more turbulence, higher pressure within the vessel, and reduced blood flow. This increases the work of the heart.
• Compliance (elasticity of vessel walls) is the ability of any compartment to expand to accommodate increased content. A metal pipe, for example, is not compliant, whereas a balloon is. The greater the compliance of an artery, the more effectively it is able to expand to accommodate surges in blood flow without increased resistance or blood pressure. When vascular disease causes stiffening of arteries, called arteriosclerosis, compliance is reduced, and resistance to blood flow is increased. The result is higher blood pressure within the vessel and reduced blood flow. Arteriosclerosis is a common cardiovascular disorder that is a leading cause of hypertension and coronary heart disease because it causes the heart to work harder to generate a pressure great enough to overcome the resistance.
• Volume of circulating blood: A relationship exists between blood volume, blood pressure, and blood flow. For example, water may merely trickle along a creek bed in a dry season but rush quickly and under great pressure after heavy rain. Similarly, as blood volume decreases, blood pressure and flow decrease, but when blood volume increases, blood pressure and flow increase. Low blood volume, called hypovolemia, may be caused by bleeding, dehydration, vomiting, severe burns, or by diuretics used to treat hypertension. Treatment typically includes intravenous fluid replacement. Excessive fluid volume, called hypervolemia, is caused by the retention of water and sodium, as seen in patients with heart failure, liver cirrhosis, and some forms of kidney disease. Treatment may include the use of diuretics that cause the kidneys to eliminate sodium and water.

Cardiovascular Centers

Sympathetic stimulation increases the heart rate and contractility, whereas parasympathetic stimulation decreases the heart rate. (See Figure 6.2h for an illustration of the ANS stimulation of the heart.) Sympathetic stimulation causes the release of the neurotransmitter norepinephrine (NE), which shortens the repolarization period, thus speeding the rate of depolarization and contraction and increasing the HR. It also opens sodium and calcium ion channels, allowing an influx of positively charged ions.

NE binds to the Beta-1 receptor. Some cardiac medications (for example, beta-blockers) work by blocking these receptors, thereby slowing HR and lowering blood pressure. However, an overdose of beta blockers can lead to bradycardia and even stop the heart.

• Contractility refers to the force of the contraction of the heart muscle, which controls SV. Factors that increase contractility are positive inotropic factors, and those that decrease contractility are negative inotropic factors. Not surprisingly, sympathetic stimulation is a positive inotrope, whereas parasympathetic stimulation is a negative inotrope. The drug digoxin is used to lower HR and increase the strength of the contraction. It works by inhibiting the activity of an enzyme (ATPase) that controls the movement of calcium, sodium, and potassium into the heart muscle. Inhibiting ATPase increases calcium in heart muscle, increasing the force of heart contractions. Negative inotropic agents include hypoxia, acidosis, hyperkalemia, and a variety of medications, such as beta-blockers and calcium channel blockers.
• Preload and Afterload- Preload is, in simplest terms, the stretching of ventricles. Ventricles tend to stretch (fill with blood) and squeeze (push out blood) to distribute blood adequately. However, if too much pressure is backed up due to cardiac issues, the ventricles tend to stretch extensively, taking longer to squeeze, resulting in an abnormal contraction. Too much stretch = inability to squeeze properly. Another definition for Preload is another way of expressing end-diastolic volume (EDV). Therefore, the greater the EDV, the greater the preload. One of the primary factors to consider is filling time, the duration of ventricular diastole during which filling occurs. Any sympathetic stimulation to the venous system will also increase venous return to the heart, which contributes to ventricular filling and preload. Medications such as diuretics decrease preload by causing the kidneys to excrete more water, thus decreasing blood volume. Afterload is a fancy word for the pressure required for the left ventricle to force blood out of the body to exert during systole. In other words, it’s the effort of the ventricle squeezing. Afterload refers to the force that the ventricles must develop to pump blood effectively against the resistance in the vascular system. Any condition that increases resistance requires a greater afterload to force open the semilunar valves and pump the blood, which decreases cardiac output. On the other hand, any decrease in resistance reduces the afterload and thus increases cardiac output. Another definition of afterload is the force that the ventricles must develop to pump blood effectively against resistance in the vascular system. Any condition that increases resistance requires a greater afterload to force open the semilunar valves and pump the blood, which decreases cardiac output. On the other hand, any decrease in resistance reduces the afterload and thus increases cardiac output. The figure below summarizes the major factors influencing cardiac output. Calcium channel blockers such as amlodipine, verapamil, nifedipine, and diltiazem can be used to reduce afterload and thus increase cardiac output.

Below is a summary of the major factors influencing cardiac output. Calcium channel blockers such as amlodipine, verapamil, nifedipine, and diltiazem can reduce afterload and thus increase cardiac output.

• Viscosity of blood is a measure of the blood’s thickness and is influenced by the presence of plasma proteins and formed elements. Blood is viscous and somewhat sticky to the touch. It has a viscosity approximately five times greater than water. Viscosity is a measure of a fluid’s thickness or resistance to flow and is influenced by the presence of plasma proteins and formed elements within the blood. The viscosity of blood has a dramatic effect on blood pressure and flow. Consider the difference in flow between water and honey. The more viscous honey would demonstrate a greater resistance to flow than the less viscous water. The same principle applies to blood.
• Elasticity of vessel walls refers to the capacity to resume normal shape after stretching and compressing. Vessels larger than 10 mm in diameter are typically elastic. Their abundant elastic fibers allow them to expand as blood pumped from the ventricles passes through them and recoil after the surge. If artery walls were rigid and unable to expand and recoil, their resistance to blood flow would greatly increase. Blood pressure would rise to even higher levels, requiring the heart to pump harder to increase the volume of blood expelled by each pump (the stroke volume) and maintain adequate pressure and flow. Artery walls would have to become even thicker in response to this increased pressure.

1. A. Homeostatic Regulation of the Cardiovascular System: To maintain homeostasis in the cardiovascular system and provide adequate blood to the tissues, blood flow must be redirected continually to the tissues as they become more active. For example, when an individual exercises, more blood will be directed to skeletal muscles, the heart, and the lungs. On the other hand, following a meal, more blood is directed to the digestive system. Only the brain receives a constant blood supply regardless of rest or activity. Three homeostatic mechanisms ensure adequate blood flow and, ultimately, perfusion of tissues: neural, endocrine, and autoregulatory mechanisms.
2. Neural Regulation: The nervous system is critical in regulating vascular homeostasis based on baroreceptors and chemoreceptors. Baroreceptors are specialized stretch receptors located within the aorta and carotid arteries that respond to the degree of stretch caused by the presence of blood and then send impulses to the cardiovascular center to regulate blood pressure. In addition to the baroreceptors, chemoreceptors monitor levels of oxygen, carbon dioxide, and hydrogen ions (pH). When the cardiovascular center in the brain receives this input, it triggers a reflex that maintains homeostasis.
3. Endocrine Regulation: Endocrine control over the cardiovascular system involves catecholamines, epinephrine, and norepinephrine, as well as several hormones that interact with the kidneys to regulate blood volume.
4. Epinephrine and Norepinephrine: The catecholamines epinephrine and norepinephrine are released by the adrenal medulla and are a part of the body’s sympathetic or fight-or-flight response. They increase heart rate and force of contraction while temporarily constricting blood vessels to organs not essential for fight-or-flight responses and redirecting blood flow to the liver, muscles, and heart.
5. Antidiuretic Hormone: The hypothalamus secretes antidiuretic hormone (ADH), also known as vasopressin. The primary trigger prompting the hypothalamus to release ADH is increasing the osmolarity of tissue fluid, usually in response to a significant loss of blood volume. ADH signals its target cells in the kidneys to reabsorb more water, thus preventing additional fluid loss in the urine. This will increase overall fluid levels and help restore blood volume and pressure.
6. The renin-angiotensin-aldosterone system(RAAS) has a major effect on the cardiovascular system. Specialized kidney cells respond to decreased blood flow by secreting renin into the blood. Renin converts the plasma protein angiotensinogen into its active form—Angiotensin I. Angiotensin I circulates in the blood and is then converted into Angiotensin II in the lungs. This reaction is catalyzed by the enzyme called angiotensin-converting enzyme (ACE). ACE inhibitors, such as lisinopril, target this step in the RAAS to decrease blood pressure.

Angiotensin II is a powerful vasoconstrictor that greatly increases blood pressure. It also stimulates the release of ADH and aldosterone, a hormone the adrenal cortex produces. Aldosterone then increases the kidneys’ reabsorption of sodium into the blood. Because water follows sodium, there is an increase in the reabsorption of water, which increases blood volume and blood pressure. The illustration of the renin-angiotensin-aldosterone system and the figure below summarize the effect of hormones involved in renal control of blood pressure.

Above: The renin-angiotensin-aldosterone system

Hormones involved in renal control of blood pressure

Autoregulation of Perfusion

Local, self-regulatory mechanisms allow each region of tissue to adjust its blood flow—and thus its perfusion. These mechanisms are affected by sympathetic and parasympathetic stimulation and endocrine factors. See the figure below for a summary of these factors and their effects.

The effects of nervous, endocrine, and local controls on the vasoconstriction and vasodilation of arterioles

III. Blood Pressure and Hypertension

Blood pressure measurements are obtained using a stethoscope and a sphygmomanometer, also called a blood pressure cuff. To obtain a manual blood pressure reading, the blood pressure cuff is placed around a patient’s extremity, and a stethoscope is placed over an artery. For most blood pressure readings, the cuff is usually placed around the upper arm, and the stethoscope is placed over the brachial artery. The cuff is inflated to constrict the artery until the pulse is no longer palpable and then deflated slowly. The American Heart Association (AHA) recommends that the blood pressure cuff be inflated at least 30 mmHg above the point where the radial pulse is no longer palpable. The first appearance of sounds, called Korotkoff sounds, is noted as the systolic blood pressure reading. Korotkoff sounds are named after Dr. Korotkoff, who first discovered the audible sounds of blood pressure when the arm is constricted. The blood pressure cuff continues to be deflated until Korotkoff sounds disappear. The last Korotkoff sounds reflect the diastolic blood pressure reading. It is important to deflate the cuff slowly at no more than 2-3 mmHg per second to ensure that the absence of pulse is noted promptly and that the reading is accurate. Blood pressure readings are documented as systolic/diastolic pressure, for example, 120/80 mmHg.

Abnormal blood pressure readings can signify an area of concern and a need for intervention. Normal adult blood pressure is less than 120/80 mmHg. Hypertension is the medical term for elevated blood pressure readings of 130/80 mmHg or higher. See Table 3.2 for blood pressure categories according to the 2017 American College of Cardiology and American Heart Association Blood Pressure Guidelines. Before diagnosing a person with hypertension, the healthcare provider will calculate an average blood pressure based on two or more blood pressure readings obtained on two or more occasions.

Hypotension is the medical term for low blood pressure readings less than 90/60 mmHg. It can be caused by dehydration, bleeding, cardiac conditions, and the side effects of many medications. Hypotension can be of significant concern because it can lead to a potential lack of perfusion to critical organs.

Orthostatic hypotension is a drop in blood pressure that occurs when moving from a lying down (supine) or seated position to a standing (upright) position. When measuring blood pressure, orthostatic hypotension is defined as a decrease in blood pressure by at least 20 mmHg systolic or 10 mmHg diastolic within three minutes of standing. When a person stands, gravity moves blood from the upper body to the lower limbs. As a result, there is a temporary reduction in the amount of blood in the upper body for the heart to pump, which decreases blood pressure. Typically, the body quickly counteracts the force of gravity and maintains stable blood pressure and blood flow. In most people, this transient drop in blood pressure goes unnoticed. However, some patients with orthostatic hypotension can experience light-headedness, dizziness, or fainting. This is a significant safety concern because of the increased risk of falls and injury, particularly in older adults. Orthostatic hypotension is also commonly referred to as postural hypotension. When obtaining orthostatic vital signs, the pulse rate may also be collected. If the pulse increases by 30 beats/minute or more while the patient stands (or sits if unable to stand), this indicates a significant change.

Equipment to Measure Manual Blood Pressure

A sphygmomanometer, commonly called a blood pressure cuff, measures blood pressure while Korotkoff sounds are auscultated using a stethoscope. Below is an image of a sphygmomanometer and stethoscope.

Cuff Types and Sizes

Manual and automatic blood pressure measurement involves using a blood pressure cuff with a sphygmomanometer. Many cuff sizes are available to fit newborns, children, adults, people with small and larger arms, and people with cone-shaped arms. The cuff is typically wrapped around the upper arm. However, a cuff can also be placed on the thigh when the arm is not feasible.  When taking the measurement, ensure that the arm and wrist are supported at heart level (Nerenberg, 2018).

Automatic blood pressure cuffs are a digital way to measure blood pressure. After positioning the patient and the blood pressure cuff on the arm, press the start button on the monitor. The cuff is automatically inflated and deflates at 2 mm Hg per second. The monitor has a digital display that shows the blood pressure reading when done. Automatic cuffs can be programmed to take a series of blood pressure readings in a row. If the healthcare provider is concerned about an initial high blood pressure reading on a patient, the accuracy of the blood pressure is verified with the following actions:

• Have the patient sit in a room by themselves
• Quiet the room
• Dim the lights
• Allow the patient to sit quietly without talking
• Then, take three measurements, a few minutes apart, with the automatic cuff. The blood pressure displayed is an average of the three readings.

Patients can monitor their own blood pressure at home with an automatic digital blood pressure monitoring device. The cuff is applied around the patient’s upper arm or wrist. Like the automatic cuff noted above, the patient presses the start button, and the cuff inflates and deflates based on programmed levels displaying a digital reading. Patients are encouraged to document their blood pressure or use a device with data-recording capabilities to increase the reliability of their reported home blood pressure monitoring. These data can be shared with the patient’s primary care provider.

Arterial catheters are an invasive way to measure blood pressure. They are only used in critical care situations when continuous blood pressure monitoring and arterial blood gas draws are required. The procedure involves inserting a catheter (similar to an intravenous) into the artery. The catheter is connected to a pressure transducer and monitor that provides a digital blood pressure reading.

Cellular phone applications have been developed to measure blood pressure, but the accuracy of this technology is still being investigated.

Definition of Hypertension: High blood pressure, or hypertension, “is when the force of the blood pushing on the blood vessel walls is too high.”

Risk factors for Hypertension:

The healthcare provider assesses a patient’s cardiovascular risk factors for atherosclerosis and hypertension. These risk factors are categorized as modifiable and non-modifiable. See below for resources concerning risk factors based on “Hypertension Canada guidelines (Leung et al., for Hypertension Canada, 2017)” and “What causes Hypertension- Risk factors: “https://storymd.com/journal/pwvvoz507w-high-blood pressure/page/lzazr1lxka-high-blood-pressure-risk-factors

Blood Pressure Categories

In 2017, new guidelines from the American Heart Association, the American College of Cardiology, and nine other health organizations lowered the numbers for the diagnosis of hypertension (high blood pressure) to 130/80 millimeters of mercury (mm Hg) and higher for all adults. The previous guidelines set the threshold at 140/90 mm Hg for people younger than age 65 and 150/80 mm Hg for those ages 65 and older.

Management of Hypertension is crucial as uncontrolled hypertension may lead to:

IV. Management of Hypertension. Non-Pharmacological Interventions and Antihypertensive Medication

VI. Antihypertensive Medications

Many different medication classifications are used to treat hypertension. Understanding the different mechanisms of action for different classes of anti-hypertensives is important because patients are often on a combination of medications that work synergistically to manage blood pressure.

1. Alpha-2 Agonist

Clonidine is an Alpha-2 agonist.

2. Ace Inhibitor (Angiotensin Converting Enzyme)

Captopril is an example of an ACE (angiotensin-converting enzyme) inhibitor.

3. Angiotensin II Receptor Blocker (ARB)

Losartan is an example of an Angiotensin II receptor blocker, also known as an ARB. ARBs are similar to ACE inhibitors in that they act on the renin-angiotensin-aldosterone system (RAAS). However, the difference is that they block Angiotensin II and cause vasodilation and decreased peripheral resistance, but they are not likely to cause the cough that ACE inhibitors can.

4. Vasodilator

Hydralazine is an example of a direct vasodilator.

Another example of a vasodilator is Nitroglycerin, which causes arterial and venous vasodilation. It is used for patients with angina to decrease cardiac workload and increase the amount of oxygen available to the heart. By causing vasodilation of the veins, nitroglycerin decreases the amount of blood returned to the heart and thus decreases preload. It also reduces afterload by causing vasodilation of the arteries and reducing peripheral vascular resistance. By reducing preload and afterload, Nitroglycerin is also used as an antihypertensive medication.

5. Beta-1 Antagonist

Metoprolol is a selective Beta-1 blocker.

6. Class II-Beta Blocker

Class II medications are beta blockers used to decrease conduction velocity, automaticity, and the refractory period of the cardiac conduction cycle. Sotalol is a Beta-1 and Beta-2 blocker with Class III antiarrhythmic properties.

Sotalol is an example of a drug that is both a Beta-1 and Beta-2 blocker but is also a Class III antiarrhythmic properties.

An Example of a drug card: Metoprolol Medication Card

Hyperlipidemia

Cholesterol is a fat (also called a lipid) that your body needs to work properly to produce cell membranes, hormones, and Vitamin D (Martin, S. S. 2024). However, too much bad cholesterol can increase the risk of heart disease, stroke, and peripheral vascular disease. The medical term for high blood cholesterol is hyperlipidemia.

There are many types of cholesterol.

There are many types of cholesterol:

• Total cholesterol: All the cholesterols combined
• High-density lipoprotein (HDL) cholesterol is often called “good” because it promotes excretion. Exercise helps to increase HDL and remove cholesterol from the bloodstream
• Low-density lipoprotein (LDL) cholesterol: Often called “bad” cholesterol because it stores cholesterol in the bloodstream, which contributes to atherosclerosis

The table below identifies normal from abnormal levels of cholesterol:

National Cholesterol Education Program Guidelines, 2018

Dietary and other lifestyle changes, including exercise, are the initial approach to lowering cholesterol.

Antilipemic Medications

Antilipemic agents reduce hyperlipidemia, which may lead to additional health problems such as stroke, myocardial infarction, angina, and heart failure. Medications should be used in conjunction with a healthy diet and exercise regime approved by the patient’s healthcare provider.

Class off Antihyperlipidemic medications include:

Statins (Lipitor®, Crestor®, Zocor® and others).

•  These drugs decrease the amount of cholesterol made by the liver and are already in the blood, and there is evidence that they may reduce inflammation in the artery walls.

PCSK9 inhibitors (Praluent®, Repatha® and Leqvio®).

• PCSK9 is a protein found in the liver that regulates cholesterol metabolism. More specifically, it stops the breakdown of LDL, leading to familial hypercholesterolemia. Therefore, the PCSK9 inhibitors decrease cholesterol by clearing LDL cholesterol.

Fibric acid derivatives or fibrates (Tricor®, Lopid®, Antara® and others).

• “Decrease low-density lipoprotein cholesterol (LDL-C), total cholesterol, triglycerides, and apolipoprotein B and increase high-density lipoprotein cholesterol (HDL-C-good cholesterol) (Matthew, C. T. & Paramvir, S 2023).”
  • It must be used with low cholesterol – low-fat diet and exercise.

Bile acid sequestrants or bile acid resins (Colestid®, Questran®, Locholest®, and others).

• Reduces cholesterol by stopping the production of bile acids, which, if produced, increases cholesterol. It lowers LDL-C. An insoluble complex is formed, and all the medication taken is excreted in the feces and bile acids removed from the enterohepatic circulation (Lent-Schochet, D. & Jialal, I. 2023). Certain medications in this class of drugs can be used by children and adolescents

Nicotinic acid or niacin (Niacor® and Niaspan®).

• This is Vitamin B3 that may boost levels of good HDL cholesterol, modestly lowering bad LDL cholesterol and lower triglycerides. May be prescribed with statins for cholesterol control (Greenwood, B.G., Griffin, R. G., Gopal, A. 2024)

Selective cholesterol absorption inhibitors (Zetia® and Nexlizet®).

• It prevents the uptake of cholesterol from the small intestine to the circulatory system by binding to bile acids and preventing the creation of new cholesterol. These medications are formulated as viscous soluble fiber or fiber supplements.

Omega-3 fatty acids and fatty acid esters (Epanova®, Lovaza®, and others).

• It lowers triglyceride levels, raises HDL cholesterol, and lowers blood pressure. This synergistic effect decreases the risk of heart disease and stroke.

Adenosine triphosphate-citrate lyase (ACL) inhibitors (Nexletol® and Nexlizet).

• These are a new class of drugs that work by inhibiting the enzyme ACL, which then inhibits the HMG-CoA enzyme. This decreases the formation and use of formerly produced circulating cholesterol. Additionally, these drugs help the body rid itself of some LDL cholesterol.

Examples of widely used Antilipemic include:

1. An example of a Statin is Atorvastatin

2. An example of a Selective Absorption Cholesterol Inhibitor is Ezetimibe

An example of an antilipemic medication Card

Now, let’s take a closer look at the medication card for atorvastatin.

Monotherapy rarely works to manage hypertension, especially if blood pressure readings are greater than is seen in Stage 1 hypertension. Approximately 70% of patients treated for hypertension need at least two different classes of antihypertensives to effectively treat their hypertension. New data indicates that dual therapy is appropriate for initial therapy.  The drugs most commonly used in combination therapy include diuretics and β-blockers, angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor antagonists, and ACE inhibitors and calcium antagonists. An anti-lipidemic may also be needed to protect the patient from cardiac disease and even stroke.

Combination therapy enables several perks, including;

1. A distinct decrease in blood pressure readings
2. A decrease in the side effect profile as lower doses of both medications are used to treat the patient.
3. Adherence to the medication plan increases.
4. A decrease in cost is noted.

V. Conditions and Disorders Related to Perfusion/Uncontrolled Hypertension

Edema

Despite valves within larger veins, some blood will inevitably pool in the lower limbs over a day due to the pull of gravity. Any blood that accumulates in a vein will increase the pressure within it. Increased pressure will promote the flow of fluids out of the capillaries and into the interstitial fluid. The presence of excess tissue fluid around the cells leads to a condition called edema. Here is an image of a patient with pitting edema.

Most people experience daily fluid accumulation in their tissues, especially if they spend much time on their feet (like most health professionals). However, clinical edema goes beyond normal swelling and requires medical treatment. Edema has many potential causes, including hypertension and heart failure, severe protein deficiency, and renal failure. Diuretics such as furosemide are used to treat edema by causing the kidneys to eliminate sodium and water.

Arteriosclerosis

Arteriosclerosis begins with injury to the endothelium of an artery, which may be caused by irritation from high blood glucose, infection, tobacco use, excessive blood lipids, and other factors. Injured artery walls cause inflammation. As inflammation spreads into the artery wall, it weakens and scars it, leaving it stiff. Circulating triglycerides and cholesterol can seep between the damaged lining cells and become trapped within the artery wall, where leukocytes, calcium, and cellular debris join them. Eventually, this plaque buildup can narrow arteries enough to impair blood flow. The term for this condition, atherosclerosis, describes the plaque deposits. See below for an illustration of atherosclerosis.

Atherosclerosis

Sometimes, plaque can rupture, causing microscopic tears in the artery wall that allow blood to leak into the tissue on the other side. When this happens, platelets rush to the site to clot the blood. This clot can further obstruct the artery and—if it occurs in a coronary or cerebral artery—cause a sudden heart attack or stroke. Alternatively, plaque can also break off and travel through the bloodstream as an embolus until it blocks a more distant, smaller artery.

Even without total blockage, narrowed vessels lead to ischemia (reduced blood flow to the tissue region “downstream” of the narrowed vessel). Ischemia can lead to hypoxia (decreased supply of oxygen to the tissues), causing a myocardial infarction or cerebrovascular accident.

The treatment of atherosclerosis includes lifestyle changes, such as weight loss, smoking cessation, regular exercise, and a diet low in sodium and saturated fats. Antilipemic drugs, such as Atorvastatin, are prescribed to reduce cholesterol and help prevent atherosclerosis.

Coronary Artery Disease

Coronary artery disease is the leading cause of death worldwide. It occurs when atherosclerosis within the walls of the coronary arteries obstructs blood flow. As the coronary blood vessels become blocked with plaque, the flow of blood to the tissues is restricted, causing the cardiac cells to receive insufficient amounts of oxygen, which can cause pain called angina. Figure 6.3 (see below) shows the blockage of coronary arteries highlighted by the injection of dye. Some individuals with coronary artery disease report pain radiating from the chest called angina, but others, especially women, may remain asymptomatic or have alternative symptoms of neck, jaw, shoulder, upper back, or abdominal pain. If untreated, coronary artery disease can lead to myocardial infarction (heart attack). Risk factors include smoking, family history, hypertension, obesity, diabetes, lack of exercise, stress, and hyperlipidemia. Treatments may include medication, changes to diet and exercise, a coronary angioplasty with a balloon catheter, insertion of a stent, or a coronary bypass procedure.

Myocardial Infarction

Myocardial infarction (MI) is the medical term for what is commonly referred to as a “heart attack.” It results from a lack of blood flow and oxygen to a region of the heart, resulting in the death of the cardiac muscle cells. An MI often occurs when the buildup of atherosclerotic plaque blocks a coronary artery and becomes a thrombus or when a portion of an unstable atherosclerotic plaque travels through the coronary arterial system and lodges in one of the smaller vessels.

In the case of acute MI, there is often sudden pain beneath the sternum (retrosternal pain) called angina, often radiating down the left arm in male patients but not as commonly in female patients. In addition, patients typically present with difficulty breathing and shortness of breath (dyspnea), irregular heartbeat (palpitations), nausea and vomiting, sweating (diaphoresis), anxiety, and fainting (syncope), although not all of these symptoms may be present. Many of the symptoms are shared with other medical conditions, including anxiety attacks and simple indigestion, so accurate diagnosis is critical for survival.

An MI can be confirmed by examining the patient’s ECG, which frequently reveals ST and Q component alterations. Immediate MI treatments are required, including administering supplemental oxygen, aspirin, and nitroglycerin. Longer-term treatments may include injections of thrombolytic agents, such as the tissue plasminogen activator, also known as tPA, that dissolve the clot; the anticoagulant heparin; a balloon angioplasty with stents to open blocked vessels; or bypass surgery to allow blood to pass around the site of the blockage. Please note that drugs such as tPA are used in Emergency and Intensive Care Units.

Cerebrovascular Accident (CVA)

The internal carotid and vertebral arteries are the two primary blood suppliers to the human brain. Given the brain’s central role and vital importance to life, the blood supply to this organ must remain uninterrupted. However, blood flow may become obstructed due to atherosclerosis or an embolus that has traveled from elsewhere in the blood. For example, an arrhythmia called atrial fibrillation can cause clots to form in the heart and then move to the brain. When blood flow is interrupted, even for just a few seconds, a transient ischemic attack (TIA), or mini-stroke, may occur, resulting in loss of consciousness or temporary loss of neurological function. Loss of blood flow for longer periods produces irreversible brain damage or a stroke, also called a cerebrovascular accident (CVA). There are two types of cerebrovascular accidents: ischemia and hemorrhagic. Ischemic strokes are caused by atherosclerosis or a blood clot that blocks blood flow to the brain. Eighty percent of strokes are ischemic. Hemorrhagic strokes are caused by a blood vessel that ruptures and bleeds into the brain. Risk factors for a stroke include smoking, high blood pressure, and cardiac arrhythmias. Treatment of a stroke depends on the cause. Ischemic strokes are treated with thrombolytic medication such as tPA to dissolve the clot, whereas hemorrhagic strokes often require surgery to stop the bleeding.

Clinical Reasoning and Decision-Making Activity

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