Key Concept

The first thing to understand about the cardiovascular system is that the purpose of the entire system is to provide oxygenation and perfusion to the body. There are four concepts related to oxygenation and perfusion that you will see again and again. You must understand these…they are:

1. Hypoxemia: decreased oxygen concentration of arterial blood
2. Hypoxia: oxygen deficiency in body tissues
3. Ischemia: tissue not getting enough oxygen
4. Necrosis: tissue death

Overview

Cardiovascular (CV) disease is the leading cause of death in the US. Some estimates show that one death occurs every 33 seconds, and 25% of the population has CV disease. Most of the patients you see in the hospital will have some kind of cardiovascular disease (and the sad part is, it is often preventable).

Technology & Diagnostics

How is CV disease diagnosed and treated? I’m glad you asked! Though advancements are occurring all the time, the mainstays of testing and treatment are:

EGG: This is your typical electrode-based diagnostic tool. This could be as few as three leads (or electrodes) and as many as 10 (which provides 12 views, so it’s called a “12-lead”).

The electrodes create a graphic representation of the electrical impulses that the heart generates during the cardiac cycle. Don’t worry; we’ll discuss this in more detail in Med/Surg 2. Interfering factors are electrolyte imbalances and certain drugs such as digitalis, quinidine, and barbiturates (also, if your patient is brushing his teeth, this looks like V-tach! Always assess your patient BEFORE you freak out!).

Ultrasound (ECHO):  Used to evaluate the structure and function of the heart. It’s not all that accurate in patients with COPD (due to a lot of air between the heart and chest cavity) and patients who are obese.

Stress Test:  A stress test is exactly what it sounds like…the heart is tested while under stress. The first part of the test is called the “resting” portion, essentially an EGG conducted while the patient rests. The “stress” portion is done next for purposes of comparison.

Most patients will undergo the stress portion by simply walking on an inclined treadmill (in some cases, they may have to jog a little to get the heart rate up), but what about patients who are too sick or disabled to ambulate safely? Those folks can still get their stress test, but the stress is chemically induced. And yes, it should

make you a wee bit nervous because these are potent drugs! The patient is injected with a medication that will make their heart beat faster while the technician records everything on the EGG. The most commonly used medications are adenosine, dobutamine, or dipyridamole (Persantine). We’ll talk about these more in the Advanced Med/Surg section.

Angiography:  Also known as a “heart cath” or, if you want to be fancy, then call it by its full name of “cardiac catheterization.” Whatever you call it, this invasive procedure is used to

visualize the heart chambers, arteries, and great vessels. It is used most often to evaluate patients with chest pain and patients who have had a positive stress test to locate the region of coronary occlusion. It is also used to determine the effects of valvular heart disease. Most heart caths are performed from the left side, but right-sided heart caths are also regularly conducted to calculate cardiac output, measure right heart pressures, and identify pulmonary emboli. If your patient is sick, they may get both.

Radioisotope studies: Sometimes, the physician needs an even more detailed picture of what is going on in the heart…and this means you’ll be going on a road trip with your patient to Nuclear Medicine (also called “Nuc Med” by those in the know.) These are relatively non-invasive (except for the required IV) and are generally well-tolerated by the patient. Like many tests,

it does require that the patient hold still for extended periods, so if your patient has a lot of anxiety or is confused, this could be a problem!

For this test, a small amount of radioactive material is injected, and the emissions from this material are detected with the imaging device to show the distribution of blood flow to the heart and details about cardiac function. And yes, it’s pretty cool to watch!

Clot prevention: Sometimes, your patient may simply need to take clot-prevention drugs such as warfarin (Coumadin), heparin, or one of the newer anticoagulants such as Pradaxa or Xarelto.

Each has benefits and risks, but the main difference between warfarin or heparin and the newer medications is that the newer ones don’t require regular blood monitoring. Before you go and get too excited, think about it…an anticoagulant medication that doesn’t require monitoring can be hazardous. It is also important to understand that while warfarin and heparin both have antidotes, these newer drugs do not. UPDATE: A reversal agent for Factor Xa Inhibitors is now called Andexanet alfa. It’s a good thing, too.

Google Eliquis or Xarelto along with the word “hemorrhage,” and you’ll understand pretty quickly why these medications should not be taken lightly.

Clot lysis: If you recall that “lysis” refers to breaking something apart, you’ll realize this refers to the “clot-busting” drugs, also known as thrombolytics. The most commonly used medications are activase and alteplase (TPA). These drugs help to break up and dissolve clots that are occluding vessels.

Angioplasty: This invasive procedure involves placing a balloon at the stenotic area to widen a narrowed or obstructed blood vessel.

Endarterectomy: This is a surgical procedure to remove plaque material or blockage in the lining of an artery…usually the carotid artery in the neck.

Stent: The placement of a stent holds an artery open. Patients receiving stents will have to take anticoagulant medication as clots form on foreign objects.

Valve surgery:   When the heart valves are faulty, they can be repaired or replaced. The types of surgeries refer to the valve in question. For example, an AVR is an aortic valve replacement, while an MVR refers to the mitral valve. Valves are repaired or replaced when not operating optimally, as in regurgitation or stenosis. More on these issues later.

Bypass surgery:  CABG (coronary artery bypass graft) and peripheral bypass are severe surgical procedures. In a CABG (pronounced “cabbage”), arteries or veins from elsewhere in the body are grafted to the coronary arteries to bypass atherosclerotic narrowings and improve the blood supply to the heart. Peripheral arterial bypass refers to treating blockages in the vessels of the legs.

Amputation: In cases of severe vascular disease, sometimes amputation is the only available treatment.

Arterial & Venous Disorders

It is important to understand that the cardiovascular system involves two types of blood vessels: arteries and veins. You absolutely must know the implications of an arterial disease vs. a venous disease as the signs/symptoms are different, and so are the treatments. More details on this in a bit.

Examples of arterial disorders:

Atherosclerosis:               Both coronary artery disease (CAD) and peripheral artery disease (PAD) involve thickening and hardening of arterial walls. When these vessel walls harden and become thick, blood flow is impaired, so you will see problems downstream of the artery. More on the difference between PAD and PVD later on.

Hypertension: Stage 1 HTN is SBP 130-139 or DBP 80-89; Stage 2 is SBP > 139 or DBP >89. Aneurysm:        A localized abnormal blood vessel dilation (usually artery).

Raynaud’s Disease: A primary vasospastic disease of small arteries, presents as an overly exaggerated response of vasomotor controls to cold or emotion. This is most easily observed

in the hands, which will pale as the tiny blood vessels limit flow to the periphery.

Buerger’s:  This is a chronic, recurring, inflammatory vascular occlusive disease, chiefly of the peripheral arteries and veins of the extremities. Be careful not to confuse this with “Berger’s Disease,” which is something else altogether! Buerger’s is strongly associated with tobacco use, and treatment often involves amputation of the affected body part.

Examples of venous disorders:

Thrombophlebitis: Inflammation of a vein in conjunction with thrombus formation.

Emboli:                         Masses of undissolved matter present in a blood or lymphatic vessel and brought there by the blood or lymph.

Venous Stasis Ulcers:        These are ulcers in the lower leg (usually inner part of leg just above ankle). They can get pretty intense, leaving shallow wounds in the leg that are extremely difficult to heal. They are common in patients with a history of leg swelling, varicose veins or blood clots.

Lymphedema:                  An abnormal accumulation of tissue fluid in the interstitial spaces.

Cardiovascular Disease

Though CV disease is the leading cause of death in the U.S., the unfortunate thing is that there are many risk factors associated with this disease that are modifiable:

Hypertension    –    Obesity   –    Smoking   –               Hyperlipidemia  – Stress Lack of Exercise –    Diabetes –  Excess Sodium                – Alcohol

Hypertension

Hypertension (HTN) affects about 25% of the US population (50 million folks), and is staged as elevated, stage 1 hypertension and stage 2 hypertension. Any elevations in BP (above 120/80) is considered risky because there is a direct relationship to CV disease as blood pressure rises. Note that elderly people can have an increase in systolic pressure only. This is because atherosclerosis causes a loss of elasticity in the large arteries and diastolic pressure does not increase in correlation with systolic.

What does HTN do that’s so damaging? For starters, it damages the intima of the vessel wall. Recall from your anatomy course that the intima is a delicate interior lining of the vessel. As it becomes damaged, macrophages are attracted to the area, causing an increase in inflammation. This, in turn, creates more work for the heart to pump against (afterload) and can lead to CHF and cardiovascular “events” such as heart attack and stroke.

Pathophysiology of Hypertension:

Step 1: The kidneys release renin into the bloodstream, which travels to the liver and converts angiotensinogen to angiotensin I.

Step 2: Angiotensin I goes to the lungs where it is converted to angiotensin II, which is a powerful vaso- constrictor!

Normal BP

SBP: < 120 DBP: < 80 Elevated BP SBP: 120-129 DBP: < 80 Stage 1 HTN SBP: 130-139 DBP: 80-89 Stage 2 HTN SBP: > 139 DBP: > 89

Step 3: Angiotensin II then goes to the kidneys, causing aldosterone to be released. Aldosterone causes sodium and water retention. This retained sodium and water both increase blood volume and blood pressure.

Step 4: Arteriolar constriction increases peripheral vascular resistance (remember that angiotensin II is a potent vasoconstrictor!). This increase in blood volume combined with the vascular resistance work together to cause hypertension.

Studies show that the incidence of myocardial infarction increases proportionately with increases in systolic pressure over 120. Studies also show that diabetics are less at risk of CV events” when diastolic pressure is <80.

Treating Hypertension:

Lifestyle modifications are fantastic, but they won’t fix everyone’s HTN. Sadly, many people find lifestyle changes difficult to adhere to, and the consequences of leaving HTN untreated are devastating. So, most people need to be on more than one type of BP drug as each type lowers blood pressure differently. If someone is going to implement lifestyle changes, they can drop their BP 5-20 mmHg for every 10kg they lose. This is highly encouraging but requires patient participation.

Each lifestyle modification can decrease SBP by 4-5 mmHg and DBP by 2-4 mmHg:

• weight loss
• Limit alcohol intake (1 drink for the ladies, no more than 2 for the gentlemen)
• increase physical activity

Adhering to a heart-healthy diet can decrease SBP by approximately 11 mm Hg:

• low in sodium
• low in saturated fat
• Eat more fruits, vegetables, and whole grains.

The treatment for hypertension is tailored to the patient’s blood pressure and other risk factors for cardiovascular disease.

Low-risk patients with elevated BP or stage 1 HTN with low risk for cardiovascular disease typically start with lifestyle modification and have their blood pressure re-checked in 3-6 months. They should be counseled on smoking cessation, dietary changes, exercise, and alcohol use.

Patients with stage 1 HTN who are at higher risk for cardiovascular disease are treated with lifestyle modifications and antihypertensive medication. The initial first-line medication is either a thiazide diuretic, CCB, ARB or ACEi. BP is checked again after one month of starting medication.

Patients with stage 2 HTN are treated with lifestyle modification and two or more antihypertensive medications from different drug classes; they should see their primary care provider one month after starting the medication.

Obesity

Obesity is associated with an increased risk of CV disease. This is especially true for “central obesity,” which is when the extra weight is carried around the abdominal area and the vital organs of the trunk. Note that obesity is an independent risk factor for HTN, but it is often associated with other risk factors such as Type 2 diabetes, inactivity, and hyperlipidemia. The dangers of obesity are very real…one study followed 1 million Americans for 14 years and found the risk of CV death to be 2x higher in obese individuals.

According to the CDC’s 2018 data:

• The prevalence of obesity among adults was 39.8%
• The annual medical costs associated with obesity were $147 billion
• Obesity-related conditions account for some of the leading causes of premature death in the US
• Hispanics and non-Hispanic blacks have a higher prevalence of obesity than non-Hispanic whites and non-Hispanic Asians

Smoking

According to the CDC, as of 2015, 15.1% of adults in the US continue to smoke, but this is down from 42% in 1965, when the CDC started tracking the data. So, while we are definitely doing better, we’re not there yet.

Smoking is the strongest promoter of atherosclerosis…how does this happen, you ask? In general terms, smoking increases peripheral vascular resistance (PVR), increases LDL (“lethal” cholesterol), and decreases HDL (“healthy” cholesterol). The arterial endothelium is damaged, and platelets (which have increased aggregation due to smoking) are thought to adhere to subendothelial connective tissue exposed by endothelial denudation, initiating the smooth muscle proliferation that leads to atherosclerotic plaque formation. Whew! That’s a mouthful! The short answer is that smoking leads to atherosclerosis!

What’s more, as many as 30% of coronary heart disease (CHD) deaths in the US each year are attributed to smoking, and the risk is strongly dose-related. It also nearly doubles the risk of ischemic stroke because the carbon monoxide more readily binds to hemoglobin than does oxygen, and tissues suffer from a lack of oxygen. What’s the takeaway here? Encourage your patients to stop smoking!

Some facts regarding smokers who have had a myocardial infarction:

• If the person quits smoking now, they have a 50% reduction in the risk of re-infarction, sudden cardiac death and total mortality
• This group is highly receptive to teaching, so teach!
• When MI patients are given information about quitting, there is a 50% long-term cessation rate, which is awesome!
• Modest telephone-based counseling can increase this percentage to 70% and is cheap!

Smoking Cessation

• Approximately 1.3 million quit each year.
• After 1 year off cigarettes, the excess risk of heart disease is reduced by half.
• After 15 years of abstinence, the risk is similar to that of people who never smoked.
• In 5-15 years, the risk of stroke returns to the level of those who have never smoked.
• Only 50% of smokers seen in primary care were spoken to about smoking.
• It is better to have a “quit day” than to taper.
• Hypnosis is not supported by sufficient evidence.
• Vaccines have been tested, perhaps someday!

• Counseling works!
• Drugs work! Nicotine patch or gum, bupropion, varenicline (Chantix).
• Chart all smoking cessation teaching
• Smoking is the cause of more than 10% of CV deaths.
• Smoking costs the US $90 billion a year.

Environmental smoke has about 34% of the impact on atherosclerotic progression that occurs with active smoking.

Hyperlipidemia

Generally, low-density lipoproteins (LDL) are the “bad” kind of lipid or cholesterol. An easy way to remember this is that L stands for “lethal.” Generally, each 1% drop in LDL confers to a 2% reduction in CV events. Note that there are two types of LDL: The small dense type (which contributes to CV disease) and the large “fluffy” type. This

probably won’t come up, but more research is being done in this area, so I thought I’d put it out there. High-density lipoproteins (HDL) are the “healthy” ones. When you look at someone’s total cholesterol level, you want to consider the ratio between their HDL and the LDL. You are good to go if LDL is low and HDL is high!

Treating Hyperlipidemia

The chosen treatment depends on several factors, including lipid profile/levels, other CV risks, and the cost of therapy. Generally, patients are advised to change their diet (low-fat, low cholesterol), adopt healthy lifestyle changes, and take drugs (statins, resins, fibrates, niacin).

Stress

Stress plays a huge role in cardiovascular risk. In fact, high stress can DOUBLE the risk of CV morbidity. That’s huge! This is a

tough one because it’s not enough just to tell patients to “chill out” or relax. Many people will need help learning healthy ways to cope with stress. This can be through meditation, exercise, deep breathing, behavioral therapy or improved communication. What you want to avoid is patients de-stressing in unhealthy ways such as smoking, drinking, binge eating, or using drugs.

Lack of Exercise

Sadly, 60% of Americans are sedentary. Physical inactivity is another one of those independent risk factors for CV disease. Improving activity reduces weight, improves lipid profiles, and reduces BP.

The NIH recommends that adults partake in 30 minutes of moderate activity five days a week for 2.5 hours. Adding moderate to vigorous activity for 60 minutes most days of the week is recommended to help adults avoid gradual weight gain.

Diabetes

Interestingly, the goal is not to keep patients’ blood glucose at “the right level,” as this historically leads to too many incidents of hypoglycemia. Instead, the goal is to keep patients closer to 70-130 when they’re not sick and usually under 150 when they’re in the hospital. This is because blood sugar levels rise when the body is under stress, and since overshooting the goal can be dangerous, we just let it ride a little higher. One of the problems diabetics have as it relates to the cardiovascular system is arterial perfusion, which leads to necrotic tissues in the periphery. You will see that many diabetics have poor tissue perfusion, poor wound healing, and fragile skin.

Sodium Intake

In obese patients, each 2g increase in sodium intake is associated with a 61% increase in CV mortality.

Alcohol Intake

And now for some good news! Moderate alcohol consumption (identified as 1 glass of wine for women and 2 glasses for men) increases HDL, may decrease coagulation, and lower blood pressure. However, moderation is the key. Large alcohol intake increases blood pressure and the risk of stroke, cardiomyopathy, and non-cardiac disorders. Note that binge drinking is a serious problem, especially among college-aged males.

Non-Modifiable Risk Factors

Unfortunately, a few risk factors are outside our control…these are gender, age, and genetics. Males are more likely to have CVD than females, and the older you get, the higher the chance. Genetics is simply the luck (or lack of it) of the draw.

Atherosclerosis

Atherosclerosis occurs when fatty plaques accumulate within the vessel wall, causing the opening to narrow. This decreases the elasticity of the vessel and reduces the blood volume that can flow through the vessels. This leads to ischemia and, in severe cases, necrosis. In chronic atherosclerosis, the individual develops collateral circulation (think of this as branches of vessels) that enable the tissues to get blood flow via an alternate route. Note that this takes time to develop. In cases of acute atherosclerosis, the effects are often more pronounced as collateral circulation has not yet developed.

Congestive Heart Failure

Congestive heart failure (CHF) occurs when the heart is not able to pump adequately to meet metabolic demands. As the heart pump fails, blood pressure drops, cardiac output drops, blood backs up into places where it shouldn’t be, and the patient feels fatigued and/or short of breath. There are two kinds of CHF: right-sided and left-sided. Understanding the pathophysiology and signs/symptoms is important, so let’s do a quick overview.

Left or Right?

In order to understand the concept of left vs right-sided heart failure, you must think about the pathway of blood flow through the body.

1. Blood is pumped out of the left ventricle into the body.
2. Blood travels to the periphery and back around to the right atrium, then right ventricle.
3. Blood is pumped out of the right ventricle into the lungs.
4. Oxygenated blood flows into the left atrium and then the left ventricle.
5. Blood is pumped out of the left ventricle into the body…. and around and around we go.

So think about what would happen in left heart failure. The blood is supposed to be pushed out to the body, but instead it backs up. Where is it going to back up to? Well, what’s on the pathway BEFORE the blood goes into the left side of the heart? The lungs! You got it! So, in left heart failure, the blood backs up to the lungs causing pulmonary edema. Because fluid gets into the alveoli and reacts with the surfactant, you get foamy sputum. The foam is basically the detergent (surfactant) mixed with fluid. You won’t see this all the time, so don’t discount left heart failure if you don’t see it. The most common symptom you will see is shortness of breath with decreased O2 saturation levels, and you’ll probably be able to hear that the lungs sound “wet.”

Now, for right heart failure. again, think about the pathway. Blood travels from the periphery to the right side of the heart. So,

if the right heart fails, you get peripheral edema and a tender/enlarged liver (called “congestive hepatomegaly”) that occurs when the hepatic veins become engorged.

The most common cause of right-sided heart failure is actually left-sided heart failure, so it’s always possible that your patient has both. If they do, they are probably in a pretty bad way. This occurs because when left-sided heart failure is present, blood backs up so much that it backs all the way into the right ventricle, and so on and so forth. Think about the pathway and it all makes absolute perfect sense.

The most common symptoms of CHF are dyspnea and fatigue

Risk Factors and Etiology of CHF

Heart failure may result from a primary abnormality of the heart muscle (such as an infarction) that impairs ventricular function and prevents the heart from pumping enough blood. It can also be caused by other problems:

• Mechanical disturbances in ventricular filling during diastole (due to blood volume that’s too low for the ventricle to pump) occur in mitral stenosis secondary to rheumatic heart disease or constrictive pericarditis and in atrial fibrillation.
• Systolic hemodynamic disturbances (excessive cardiac workload caused by volume overload or pressure overload) limit the heart’s pumping ability. This can result from mitral or aortic insufficiency, which leads to volume overload.

It can also result from aortic stenosis or systemic hypertension, which causes increased resistance to ventricular emptying and decreased cardiac output.

• Myocardial infarction.
• Lung disease decreases oxygen saturation levels, so the body compensates by vasoconstricting the vessels in the lungs. This causes a lot of resistance for the right side of the heart to pump against, and it gets into trouble, leading to right-sided heart failure.

Ventricular Function

How well the ventricle pumps depends on several factors:

1. Contractility: How well does the heart contract? Contractility directly affects stroke volume, which affects cardiac output. Recall that heart rate x stroke volume = cardiac output
2. Preload: How much blood is delivered to the heart (venous return)? If you are dehydrated, this will cause low preload, so you need to give that person fluids. Preload also affects stroke volume (and thus cardiac output).
3. Afterload: Is the heart pumping against a lot of pressure? If so, stroke volume will go down.
4. Heart rate: Elevated heart rates mean less time for ventricular filling, so cardiac output will be reduced.
5. Left ventricle wall integrity, synergistic left ventricle contraction and valvular competence are all related to cardiac output. If any of these factors are not operating well, cardiac output will be reduced.

Classification of CHF (based on symptoms)

CHF can range from asymptomatic left ventricular (LV) dysfunction all the way to refractory CHF (“refractory” simply means anything that is resistant to treatment). If we treat CHF early before symptoms appear, we have a better chance of treating the disease overall. You may hear these classes referred to as the patient’s “functional capacity.”

Normal heart:       Has no symptoms, has normal exercise ability and normal left ventricle function.

Class I:              Asymptomatic. Has no symptoms, normal exercise response with abnormal left ventricle function.

The ejection fraction (EF) may be down, but you’d only know this if you did an ECHO. Class II:       Compensated. Has no symptoms unless exercising, left ventricle function is abnormal. Class III:           Decompensated. Has symptoms when not exercising, left ventricle function is abnormal.

Class IV:             Refractory. Has symptoms that are not controlled with treatment. This guy needs a heart transplant.

Classification of CHF (based on assessment of patient)

Class A:              No evidence of disease, no symptoms, and no limits on physical activity.

Class B:             Minimal cardiovascular disease. Mild symptoms and slight limitation during ordinary physical activity, but patient is comfortable while resting.

Class C:             Moderately severe cardiovascular disease. Very limited in regards to activity (even light activity), however patient is comfortable while resting.

Class D:             Severe cardiovascular disease. Severely limited in regards to activity, patient has symptoms even while resting.

CHF Treatment Objectives

The goals with treating CHF are to increase survival, decrease morbidity, increase exercise capacity, increase quality of life, decrease neurohormonal changes, halt progression of the disease (or at least slow it) and decrease symptoms. The reason you want to decrease neurohormonal changes is because when blood pressure is low, the neurohormonal response activates the SNS, which stresses the heart. So, the heart remodels which means it gets fibrous tissue. Unfortunately, fibrous tissue does not work as well so we will turn off the neurohormonal response with medications to prevent fibrosis in the heart. What meds do we use to accomplish this? ACE-inhibitors and Beta Blockers.

Treatments for CHF

The main goal with CHF is to correct aggravating factors:

• Pregnancy (symptoms often resolve after giving birth)
• Arrhythmias such as atrial fibrillation
• Infections

Increased Risk for CHF arrhythmias bradycardia pregnancy thyrotoxicosis

pulmonary embolism infections anemia

increased physical activity increased salt intake increased water intake emotional stress

failure to comply with therapy

• Hyperthyroidism
• Thromboembolism
• Endocarditis
• Obesity
• Hypertension
• Physical activity
• Dietary excess
• Medications (more on this in a moment)

In terms of treatment, it depends on the severity of the disease. It is classified by the New York Heart Association as Class

1. , based on the ability of the patient to exercise without symptoms. It is staged based on evolution of the disease on a letter scale A through D (see above). How we treat it combines both of these assessments together:

• Class A is the individual who is at high risk, but not actually showing signs. The goal here is to lower the risk and we do this by giving an ACEi.
  • B is for anyone who has asymptomatic LV dysfunction, an EF < 40% (class I). This person will get an ACEi and a B-Blocker in an effort to reduce risk.
  • C is for symptomatic CHF (class II and III). This person will get an ACEi, a B-Blocker, diuretics and be on a low sodium diet…all in an effort to reduce risk. They may also get an ARB (angiotensin II receptor blocker) and digoxin.
  • D is for the most at-risk person…symptomatic CHF (class IV). This person will get specialized therapy and get in line for a heart transplant.

Common Clinical Findings of CHF

dyspnea – fatigue – cheyne stokes respirations orthostatic hypotension – liver tenderness – liver enlargement

peripheral edema – pulmonary crackles – weak pulses

QUIZ TIME! A 62-year-old tests negative for a heart attack. Her BP is 151/84, and she has an EF of 35%. She exhibits no signs of dyspnea and does yoga three times a week. What meds would you anticipate this patient is prescribed?

Medications for Treating CHF

What is an Ejection Fraction?

An “ejection fraction” or “EF” measures the percentage of blood leaving the heart each time it pumps. It shows how well the heart pumps with each beat. A normal LVEF is 55-70%.

ACE inhibitors (ACEi)

ACE inhibitors inhibit the renin-angiotensin-aldosterone system. Recall that this system is activated in response to hypotension, decreased sodium concentration in the distal tubule, decreased blood volume and renal sympathetic nerve stimulation.

The kidneys release renin, which cleaves angiotensinogen into angiotensin I. Angiotensin I is then converted into angiotensin II via the angiotensin-converting enzymes (ACE) in the lungs (also in the endothelium of blood vessels in many body parts). Angiotensin II causes vasoconstriction and the release of ADH (among other things).

Both of these work to increase blood pressure. If this pathway is inhibited, the increase in blood pressure is thus inhibited. That’s what an ACEi does.

ACEi drugs end in the word “pril”. Quinapril was studied in 1993 and the study shows that patients who received quinapril

did not require any additional treatment, as compared to the group who took quinapril for a while and then took a placebo. Lisinopril is one of the more common ones you’ll see these days.

The advantages of ACEi are:

• Inhibit left ventricular remodeling post myocardial infarction (remember that ACEi block the “neurohormonal pathway” introduced earlier)
  • Modify the progression of chronic CHF (increased survival and decreased hospitalizations; improved quality of life)
  • In contrast to other vasodilators, do not produce neurohormonal activation or reflex tachycardia
  • Tolerance to its effects does not develop
  • Studies show that the probability of death decreases when taking ACEi vs a placebo

ACEi indications are:

• Clinical cardiac insufficiency (all patients)
  • Asymptomatic ventricular dysfunction (LVEF < 35%)
  • High risk CHF patients (those with diabetes, hypertension, atrioventricular septal defect, or anyone who’s had a myocardial infarction).

Angiotensin I Inhibitors (also known as AT1 receptor blocker, or ARB)

These drugs block vasoconstrictor and aldosterone-secreting effects of angiotensin II at various receptor sites including vascular smooth muscle and the adrenal glands. It leads to vasodilation and lowers blood pressure. Some common ARBs are Losartan, Valsartan, Irbesartan and Candesartan. Notice they end in “-sartan”.

Diuretics (Thiazides, Potassium-Sparing, and Loop)

Thiazides act on the cortex of the kidney. They inhibit active exchange of Cl and Na in the cortical diluting segment of the ascending loop of Henle. They increase the excretion of sodium and water by inhibiting sodium reabsorption. In the process, hydrogen ions are also excreted, which can contribute toward metabolic alkalosis. Remember that water follows salt, so if we excrete sodium, we also excrete water. The most common one you will see is Hydrochlorothiazide.

Potassium-sparing diuretics act on the medulla and inhibit reabsorption of Na in the distal convoluted and collecting tubule. They also save K, so you will want to make sure K is not too high. They also save hydrogen ions, so metabolic alkalosis is less of an issue. Spironolactone is a common one you’ll see.

Loop diuretics act on the medulla and inhibit the exchange of Cl, Na, K in the thick segment of the ascending loop of Henle. Note that hydrogen ions are also lost with loop diuretics as well. A common loop diuretic is Lasix (furosemide).

With both thiazide and loop diuretics, you absolutely must watch for hypokalemia. If your patient is given one of these medications and excreting a lot of urine (and with it a lot of potassium), their levels can drop leading to cardiac arrhythmias.

Digoxin

Digoxin binds to the Na/K/ATPase pump in the membranes of heart cells and de-

Remember This! Beta blockers end in “olol” ACEi end in “pril”

ARB end in “sartan”

creases its function. This causes an increase in the level of sodium ions in the myocytes which then leads to a rise in the level of calcium ions. This causes an increase in the length of Phase 4 and Phase 0 of the cardiac action potential, which when combined with the effects of digoxin on the CNS, leads to a decrease in heart rate.

Increased amounts of calcium are then stored in the sarcoplasmic reticulum and released by each action potential, which is unchanged by digoxin.

This leads to increased contractility of the heart. Digoxin also increases vagal activity via its action on the CNS, decreasing the

conduction of electrical impulses through the AV node. Whew! The short version is that digoxin makes the heart beat more slowly and stronger:

• Increases the force of myocardial contraction
  • Prolongs refractory period of the AV node
  • Decreases conduction through the SA and AV nodes
  • Causes increased cardiac output and slowing of the heart rate

However, don’t go thinking digoxin is the holy grail of CV medications. The long-term effects are mixed:

• Survival similar to that of the placebo
  • Fewer hospital admissions
  • More serious arrhythmias
  • More myocardial infarctions

Digoxin Toxicity NCLEX (and nursing schools) love to ask questions about digoxin toxicity. The question will usually be about someone with a bradycardia who is nauseous/vomiting and seeing yellow.

These are classic signs of digoxin toxicity. The treatment is a drug called Digibind, which is really really expensive…

about $700 per vial.

Vasodilator Drugs

Vasodilators affect preload and afterload. There are different kinds of vasodilators:

Arterial vasodilators reduce arterial pressure by decreasing systemic vascular resistance. This benefits patients in heart failure by reducing the afterload on the left ventricle, which enhances stroke volume and cardiac output and leads to secondary decreases in ventricular preload and venous pressure. Patients with angina benefit from arterial dilators because they decrease the oxygen demand of the heart, thereby improving the oxygen supply/demand ratio. Ex: Minoxidil, Hydralazine.

Venous vasodilators reduce venous pressure, which reduces preload on the heart thereby decreasing cardiac output and the workload of the heart. This also decreases proximal capillary hydrostatic pressure, which reduces capillary fluid filtration and edema formation (edema is a result of heart failure). Ex: Nitroglycerin (which is a nitrate).

To sum up…nitrates have several different effects:

• Venous vasodilation (reduce preload leading to reduced pulmonary congestion, reduced ventricular size, reduced ventricular wall stress and reduced venous oxygen saturation)
  • Coronary vasodilation increases myocardial perfusion (which is why it is often given when patients are experiencing chest pain).
  • Arterial vasodilation decreases afterload, leading to decreased cardiac output and blood pressure.

Tolerance to Nitrates

After being administered nitrates, patients begin to experience nitrate tolerance. This is a decrease in the effectiveness of the drug. This tolerance develops with all nitrates and is dose-dependent. However, it decreases in 24 hours after stopping the drug. The good news is that tolerance can be avoided if you administer nitrates at the lowest possible dose and create discontinuous plasma levels. You’ll notice that when administering nitrates, you’ll often be instructed to apply the nitro paste

for some time, remove it, and then reapply it. So, when you see that your patient has a “drug-free” period here and there, that’s why.

When giving nitrates, you want to monitor the patient’s blood pressure. If the blood pressure is low, you’ll likely hold the dose.

If the blood pressure drops while the medication is being administered, you will stop the infusion (if running through IV) or wipe off the paste (if administered transdermally). Be careful that you don’t touch the paste as you will get an intense headache (often referred to as a “nitro headache.”)

Aldosterone Inhibitors

In addition to being a potassium-sparing diuretic, Spironolactone is an aldosterone inhibitor. It’s not as powerful a diuretic as Lasix, but since it blocks aldosterone, it helps decrease fibrous tissue formation (remodeling). Note that since this drug con- serves potassium, you will want to talk to the MD about holding the drug if your patient becomes hyperkalemic.

Beta-Blockers

Carvedilol is a common beta blocker used to treat heart failure. As the name suggests, beta blockers block beta-1 (myocar- dial) and beta-2 (pulmonary, vascular, uterine) adrenergic receptor sites. It also has alpha-1 blocking activity which means it may result in orthostatic hypotension. Be careful when getting this patient out of bed!

Therapeutic effects are decreased heart rate and blood pressure, improved cardiac output, slowing of the progression of CHF and decreased risk of death. Yay!

Survival of patients on beta blockers is pretty darn good. Basically, if people are on beta blockers and ACEi, the mortality rate goes down to 13.3% (a decrease from 27.7%).

Anticoagulants

Anticoagulants are given for a variety of reasons:

• Previous embolic episode
  • Atrial fibrillation
  • Identified thrombus
  • Left ventricular aneurysm (3-6 months post MI)
  • Class III-IV CHF in the presence of an EF less than 30%, and/or an aneurism or a very dilated left ventricle.
  • Phlebitis (inflammation of a vein)
  • Prolonged bed rest

Nursing Interventions for CHF

Assist with ADLs:              This patient is going to be fatigued

Improve SOB:                  Raise HOB up, administer O2, give meds to decrease preload & afterload Keep an eye on K:    Know how the meds affect K levels, keep an eye on I&O

Peripheral Vascular Disease

Peripheral Vascular Disease can be broken down into arterial and venous diseases. Your exams will ask you to differentiate between arterial and venous disorders, so learn how to keep these straight. In general, here’s what to look for when you are determining arterial vs. venous:

Skin Characteristics

• Arterial:            Dependent rubor, pallor with elevation, hypertrophied toenails, cool skin, hairless extremity, tissue atrophy; ulcers very painful
  • Venous:           Red color to skin, induration, warmth, tough skin; ulcers moderately painful and usually located on the medial ankle.

Pain

• Arterial:            Typically brought on by exercise and relieved by rest (intermittent claudication); sometimes unremitting pain in foot even at rest; sharp and stabbing
  • Venous:           Tenderness along vein, discomfort may be relieved by applying heat; cramping and aching, walking/activity may help

Pulses

• Arterial:            Weak or absent
• Venous:           Typically present

Surrounding tissue

• Arterial:            Gangrene, delayed wound healing
  • Venous:           Edematous, itchy and scaly skin, thick/coarse/brownish skin around the ankles

Assessment for PVD is to check for CSM: circulation, sensation and movement. You will monitor for the 5Ps, which are pain, pallor, pulselessness, paresthesia and paralysis. If your patient has any of these signs, notify the MD STAT as the patient may be losing blood flow to the limb and possibly needs immediate intervention to restore perfusion.

To manage peripheral vascular disease we’re going to do a few things:

• Reduce risks
  • Clot prevention/dissolution
  • Surgery (in extreme cases)

Aneurysm

Aneurysms are classified based on how they are shaped.

• Saccular = a unilateral outpouching; has a neck and mouth
  • Fusiform = a bilateral outpouching; involves the entire circumference
  • Dissecting = a bilateral outpouching in which layers of the vessel wall separate, creating a cavity; this is not a “true” aneurysm but rather a hematoma in the arterial wall layers
  • False = the wall ruptures and a blood clot is retained in an outpouching of tissue, or there is a connection between a vein and an artery that does not close

Pathophysiology of Aneurysms

An aneurysm can be venous or arterial. The exact cause is unknown, but recent evidence includes atherosclerosis and hypertension. Genetics can also come into play such as with Marfan syndrome. Other causes of aneurysms include infection, mycotic infections and even trauma (though that last one is rare).

Clinical Manifestations of Aneurysms

• AAA (Abdominal Aortic Aneurysm)
  • It can typically be palpated in the
  abdomen once it’s at 5.
• The most common clinical manifestation is the client’s awareness of a pulsating mass in the abdomen, followed by abdominal pain and back pain. Groin pain and flank painBruits can be heard over the aneurysm. A bruit is an adventitious sound of venous or arterial origin heard on auscultationSometimes, mottling of the extremities or distal emboli in the feet alert the clinician to a source in the abdomen.
  • Ultrasonography and CT are diagnostic tools.

• Ruptured AAA
  • Pulsating sensation in the abdomen
  • Abrupt excruciating pain (ripping or knife-life back pain that radiates…this is a big one you’ll see on tests!)

Manifestations of AAA cont’d

• Manifestations of shock (pallor, tachycardia, hypotension, dry skin, excessive thirst)
  • Diminished peripheral pulses or unequal pulses
  • Abdominal rigidity
  • Differing blood pressure in arms
  • Paraplegia, hemiplegia
  • Decreased urine output or hematuria

Raynaud’s Syndrome

Raynaud’s is an arterial disease in which the small arteries and arterioles constrict in response to various stimuli. This can be caused by cold, nicotine, caffeine, and stress. Obstructive Raynaud’s is often seen with autoimmune diseases. The most common symptom is extreme paleness in the fingers and toes, often with a clear line of demarcation between the perfused and non-perfused areas.

Buerger’s Disease

Buerger’s Disease is an inflammatory disease of the small and medium-sized arteries and veins of the extremities. It appears to be directly related to smoking (reason #5,673 why smoking is bad for you). The main clinical manifestations are pain, digital ulcerations, and ischemia. Patients may also have cold sensitivity with color changes and pain. Pulses in the posterior tibial and dorsalis pedis are weak or absent, and in advanced cases, the extremities may be abnormally red or cyanotic. Ulceration and gangrene are frequent complications. If the patient doesn’t stop smoking, they are very likely to lose fingers (or whatever part is affected). This disease is hard to treat, and drugs don’t work very well.

DVT – Deep Vein Thrombosis

• Endothelial injury due to trauma or surgery
  • Circulatory stasis due to immobility
  • Hypercoagulable state

Prevention and Treatment of DVTs

• Heparin or warfarin (brand name = coumadin)
  • TEDs/SCDs (prevention only)
  • Elevation
  • Early ambulation (prevention only)

Mechanism of Action of Anti-thrombotic Agents

• Anticoagulants prevent clot formation and extension
  • Antiplatelet drugs interfere with platelet activity
  • Thrombolytic agents dissolve existing thrombi

hypercoagulable

Pulmonary Embolism

This is a very bad situation when a thrombus breaks off and travels to the lungs (where it obstructs the pulmonary arterial bed). Though it can be so mild as to produce no symptoms, a massive embolism (obstructing more than 50% of the circulation) is rapidly fatal.

What to look for:

• First sign is usually dyspnea, may be accompanied by angina or pleuritic chest pain
  • Tachycardia
  • Air hunger
  • Dropping O2 saturation
  • Feeling of impending doom (one of the most common signs!)
  • Productive cough (may have blood)
  • Low-grade fever
  • Pleural effusion

Less common signs:

• Massive hemoptysis
  • Splinting of the chest
  • Leg edema
  • Cyanosis, syncope, distended neck veins
  • Pleural friction rub
  • Signs of circulatory collapse
  • Hypoxia

Treatment/Management

• Resuscitate as needed
  • Give O2, which may need to be intubatedGive heparin or TPA
  • If can’t tolerate heparin or TPA, then surgery

Lymphedema

Lymphedema occurs when the lymphatic flow is blocked, but it can also occur with low serum protein and high venous pressure (think about the pressure gradients in the vasculature you learned in A&P.) It is treated by elevating the affected body part, compressing the affected body part, providing skin care and infection treatment, and administering diuretics.

Aging and the CV system

As we age, the efficiency of the heart’s pumping action decreases. This is related to connective tissue changes (decreased compliance), increased fat, and sclerosis, causing lower cardiac output, arrhythmias, and valve incompetence. The vasculature changes as well, with reduced elastin and increased arteriosclerosis.

Frequently Asked Questions About Cardiovascular Health

What is the function of the cardiovascular system?

Answer: The cardiovascular system circulates blood throughout the body, delivering oxygen and nutrients to cells while removing waste products.

What are the major components of the cardiovascular system?

Answer: The major components include the heart, blood vessels (arteries, veins, and capillaries), and blood.

What is atherosclerosis?

Answer: Atherosclerosis is a condition characterized by the buildup of plaque (fat, cholesterol, and other substances) on the walls of arteries, leading to narrowing and potential blockages.

What are the risk factors for cardiovascular disease?

Answer: Risk factors include high blood pressure, high cholesterol, smoking, obesity, sedentary lifestyle, diabetes, and family history.

How can cardiovascular health be maintained?

Answer: Maintaining cardiovascular health involves regular exercise, a balanced diet low in saturated fats and cholesterol, avoiding smoking, managing stress, and regular medical check-ups.

What are the symptoms of a heart attack?

Answer: Symptoms include chest pain or discomfort, shortness of breath, nausea, lightheadedness, and pain or discomfort in the arms, back, neck, jaw, or stomach.

How can nurses assist in preventing cardiovascular disease?

Answer: Nurses can educate patients on healthy lifestyle choices, assist in managing risk factors like blood pressure and cholesterol, support smoking cessation, and promote regular exercise and a balanced diet.

What are some common medications used to manage cardiovascular conditions?

Answer: Common medications include statins for cholesterol management, ACE inhibitors and beta-blockers for blood pressure control, antiplatelet drugs like aspirin for preventing blood clots, and medications for managing heart rhythm abnormalities.