Chapter 6: Pathophysiology of the Cardiovascular System · 2016-12-20 · Page 115 nursing.elitecme.com Chapter 6: Pathophysiology of the Cardiovascular System 4 Contact Hours Release

Page 115 nursing.elitecme.com

Chapter 6: Pathophysiology of the Cardiovascular System

4 Contact Hours

Release Date: 6/30/2016 Expiration Date: 6/30/2019

AudienceThis adult focused course is for all generalist nurses who care for adults. The course includes practice standards, best practices

guidelines, and therapies related to assessment and care of patients with disease of the cardiovascular system.

Purpose statementCaring for diseases of the cardiovascular system are part of every day nursing care. This course reviews the pathophysiology of the

cardiovascular system, and updates current standards and therapies. It is a vital course of contemporary best practices nursing care.

Learning objectives � Describe the anatomy and physiology of the heart. � Discuss the pathophysiology of pumping and non-pumping

diseases of the heart. � Describe the causes and etiology of pumping and non-pumping

diseases of the heart.

� Recognize signs and symptoms of pumping and non-pumping diseases of the heart.

� List three various tests used for diagnosis. � Determine pharmacologic and non-pharmacologic treatment of the

various diseases.

How to receive credit ● Read the entire course online or in print which requires a 4-hour

commitment of time. ● Depending on your state requirements you will be asked to

complete either: ○ An affirmation that you have completed the educational

activity.

○ A mandatory test (a passing score of 70 percent is required). Test questions link content to learning objectives as a method to enhance individualized learning and material retention.

● Provide required personal information and payment information. ● Complete the MANDATORY Self-Assessment and Course

Evaluation. ● Print your Certificate of Completion.

Accreditations and approvalsElite is accredited as a provider of continuing education by the American Nurses Credentialing Center’s Commission on Accreditation.

Individual state nursing approvals In addition to states that accept ANCC, Elite is an approved provider of continuing education in nursing by: Alabama, Provider #ABNP1418 (valid through April 30, 2017); California Board of Registered Nursing, Provider # CEP15022; District of Columbia Board of

Nursing, Provider # 50-4007; Florida Board of Nursing, Provider # 50-4007; and Kentucky Board of Nursing, Provider # 7-0076 (valid through December 31, 2017).

FacultyCarol Gelman, MD, MS, HC.Dr. Gelman received her medical degree in South Africa. She has now lived in the United States for the past 16 years and now considers this her home. Dr. Gelman considers medicine to be an essential part of who she is. Since arriving in the U.S., she realizes how important communication is in understanding, implementing, and working in health care. This led her to return to school for a degree in health communication from Metropolitan College, Boston. The blend of medicine and health communication has provided Dr. Gelman the perfect foundation for writing and educating. Elite is privileged to have Dr. Gelman as a course writer. In her spare time, Dr. Gelman,

who lives in Atlanta, cares for two lovely girls, aged 9 and 17, a Golden Retriever, and a stray cat. She also enjoys creating vintage digital French graphics.

Content ReviewerIrene Owen, ARNPActivity DirectorJune D. Thompson, DrPH, MSN, RN, FAEN, Lead Nurse Planner

nursing.elitecme.com Page 116

DisclosuresIn accordance with the ANCC Standards for Commercial Support for continuing education, Elite implemented mechanisms prior to the planning and implementation of the continuing education activity, to identify and resolve conflicts of interest for all individuals in a position to control content of the course activity.

Sponsorship/Commercial Support and Non-EndorsementIt is the policy of Elite not to accept commercial support. Furthermore, commercial interests are prohibited from distributing or providing access to this activity to learners.

DisclaimerThe information provided in this activity is for continuing education purposes only and is not meant to substitute for the independent

medical judgment of a healthcare provider relative to diagnostic and treatment options of a specific patient’s medical condition.

©2016: All Rights Reserved. Materials may not be reproduced without the expressed written permission or consent of Elite Professional Education, LLC. The materials presented in this course are meant to provide the consumer with general information on the topics covered. The information provided was prepared by professionals with practical knowledge of the areas covered. It is not meant to provide medical, legal, or professional advice. Elite Professional Education, LLC recommends that you consult a medical, legal, or professional services expert licensed in your state. Elite Professional Education, LLC has made all reasonable efforts to ensure that all content provided in this course is accurate and up to date at the time of printing, but does not represent or warrant that it will apply to your situation nor circumstances and assumes no liability from reliance on these materials. Quotes are collected from customer feedback surveys. The models are intended to be representative and not actual customers.

OvervIew OF tHe CArDIOvASCuLAr SyStemThe cardiovascular system centers on the heart, which pumps blood through a closed system of blood vessels. The primary function of the cardiovascular system is to transport nutrients, water, gasses, wastes, and chemical signals throughout the body [1].

The cardiovascular system consists of three parts: the heart which pumps the blood; the blood vessels via which blood flows (including the systemic and pulmonary circulation); and the blood which transports oxygen, carries nutrients, and disposes of waste products.

Anatomy of the heartThe heart is coned shaped muscular organ situated in the chest cavity between the lungs and behind the sternum. The heart is generally the size of a fist and can weigh between 250-300 grams [3].

the layers of the heartThe heart consists of three layers: the pericardium which surrounds the heart; the myocardium; and the endocardium, or heart wall. The heart wall is made up of three layers: the epicardium, the myocardium, and the endocardium [4]. The epicardium (outermost layer) is composed of coronary arteries and nerves that innervate the heart. The myocardium

(middle layer) is composed of cardiac muscle. The endocardium (innermost layer) contains the Purkinje fibers; the main function of Purkinje fibers is the conduction of electrical impulses which cause the heart to contract and relax [2].

the chambers of the heartThe heart consists of four chambers. The two upper chambers are the right and left atria and the two lower chambers are the right and left ventricles. The right ventricle pumps blood into the pulmonary

circulation. The left ventricle pumps blood into the systemic circulation. The atria and ventricles are separated by closable one way valves [2].

the heart valvesHeart valves function to ensure unidirectional flow of blood through the heart. The heart contains two types of valves: the atrioventricular valves (AV valves); and the semilunar valves.

The AV valves separate the atria from the ventricles and are the tricuspid valve on the right and the mitral valve on the left [5]. The

tricuspid valve separates the right atria from the right ventricle and the mitral valve separates the left atria from the left ventricle. The semilunar valves separate the ventricles from the major arteries. The pulmonary valve separates the right ventricle from the pulmonary artery. The aortic valve separates the left ventricle from the aorta. Normal heart sounds are caused by the closing of the heart valves [5].

the blood vesselsArteries carry blood away from the heart and veins carry blood towards the heart. Arteries have thick walls to allow them to withstand changes in blood pressure, while veins have relatively weak walls with

one way valves which assist in the movement of blood towards the heart. The exchange of substances occurs across capillaries.

Heart blood flowThe right and left sides of the heart work together simultaneously as a doublepump [5]. The right side is a pump to the pulmonary circulation and the left side is a pump to the systemic circulation. The right atrium receives deoxygenated blood from the vena cava and from the coronary veins. The right ventricle receives deoxygenated blood from the right atrium via the right AV valve (tricuspid). This deoxygenated

blood travels via the pulmonary valve to the pulmonary arteries in the lungs and becomes oxygenated in the lungs. The oxygenated blood travels via the pulmonary vein to the left atrium of the heart and flows via the left AV valve (mitral) to the left ventricle and then to the systemic circulation via the aortic valve [4].


the coronary circulationThe right and left coronary arteries lie on the surface of the heart. The coronary veins drain into the coronary sinus which then drains to the right atrium.

Pathophysiology of diseases of the heartThe heart can be considered as a double pump and diseases of the heart can be classified according to pumping and non-pumping diseases.

PumPIng DISeASeS OF tHe HeArt

Heart failure Heart failure is the inability of the heart to supply adequate oxygenated blood to the peripheral tissues and organs to meet metabolic

demands[6]. To understand heart failure, it is important to understand how the heart works [8].

terminology[8]

● Cardiac output is the volume of blood pushed out of the left ventricle per minute.

● Stroke volume is the amount of blood ejected from the left ventricle during one contraction.

● Cardiac output = stroke volume x heart rate. Cardiac output is dependent on several factors: Preload, afterload, contractility, and heart rate.

● Preload is the amount the ventricles have stretched at the end of the diastole/relaxation stage. It is also known as the left ventricular diastolic pressure (LVEDP).

● Afterload is the amount of resistance the left ventricle has to overcome to push the aortic valve open and push blood into the systemic circulation. It is also known as systemic vascular resistance.

● Contractility is the force of ventricular contraction. ● Heart rate is the number of times the heart beats per minute.

Heart rate is important because it is a major contributor to cardiac output. Normal heart rate is between 60-100 beats per minute.

Heart failure does not mean that the heart has stopped beating, but rather that the heart, which is a muscle, is not pumping properly. As

a result it is unable to pump sufficient blood to the rest of the body. As the heart muscle weakens and the pumping action of the heart decreases, blood can build up in the lungs, liver, and/or legs. This can result in shortness of breath, i.e. dyspnea, and swelling of the legs, i.e. edema. It can also result in inadequate blood supply to organs, and long-term, can lead to organ failure from lack of oxygen. Heart failure can occur acutely, but it is usually a chronic illness that develops over time [6].

Heart failure results in a cascade of compensatory mechanisms. Baroreceptors and chemoreceptors cause the activation of the sympathetic nervous system and the renin-angiotensin adotrone system. Baroreceptors monitor blood pressure and when these receptors detect a lowering of blood pressure, they stimulate the cardiac center in the brain which in turn signals sinoatrial receptors in the heart to fire more rapidly and increase contractility and heart rate. Chemoreceptors detect changes in oxygen and trigger the sympathetic nervous system, leading to an increase in adrenaline and noradrenaline, resulting in vasoconstriction. This is a physiological attempt to normalize blood pressure [6].

the renin-angiotensin aldosterone systemLack of perfusion/oxygenation of the kidneys signals the activation of the renin-angiotensin aldosterone system. Renin is released by the kidneys in response to low blood pressure and this transforms angiotensinogen to angiotensin in the liver. Angiotensinogen is a precursor protein made in the liver for a hormone called angiotensin I. Renin catalyzes a reaction that converts angiotensinogen protein into angiotensin I, which is a precursor hormone that is converted to an active hormone called angiotensin II by an enzyme known as angiotensin-converting enzyme in the lungs [65]. Angiotensin II is a

vasoconstrictor which leads to an increase in blood pressure and causes the release of aldosterone. Aldosterone promotes the reabsorption of sodium and water in an effort to increase blood pressure. ADH is released by the pituitary which causes vasoconstriction and the retention of sodium and water. Peripheral resistance is also increased, which increases cardiac output temporarily as the increase in blood pressure results in the heart having to pump even harder. The end result is further impairment of cardiac function [6].

etiology of heart failure[9]

The main causes of acute heart failure include: Severe infections such as viruses that attack the heart muscles; allergic reactions; blood clots in the lungs; certain medications; and other illnesses that affect the whole body.

The main causes of chronic heart failure include coronary artery disease (e.g. myocardial infarction/heart attack); high blood pressure; and valvular problems of the heart. Further causes of chronic heart failure are listed alphabetically: Alcohol abuse; aortic valve disease; arrhythmias; cardiac drugs (e.g. beta-blockers, calcium antagonists); cardiac tamponade; cardiomyopathy; congenital abnormalities; fever; hypertension; mitral valve disease; myocardial infarction; myocarditis;

pericardial disease; pregnancy; pulmonary heart disease; rheumatic heart disease; severe anemia; systemic lupus erythematosus; thyroid disease (especially hyperthyroidism); and tricuspid valve disease.

These conditions damage the heart muscle, making it stiff and impairing heart function. Heart failure affects contractility and/or relaxation of the heart. A decrease in contractility results in the heart being unable to push out sufficient blood to the rest of the body and/or the inability to relax sufficiently to allow for adequate filling of the ventricles.


Pathophysiology of heart failure[60]

Heart failure can be a result of right ventricular failure, left ventricular failure, or a combination of both. With left ventricular failure, there is a decrease in cardiac output, causing an increase in back pressure towards the pulmonary veins. If pulmonary capillary pressure exceeds the oncotic pressure of plasma proteins, fluid leaves the capillaries and enters the interstitial space and alveoli, causing pulmonary edema and decreasing pulmonary compliance and increasing the work of breathing. In right ventricular failure, there is an increase in systemic venous pressure; if systemic capillary pressure exceeds the oncotic pressure of plasma proteins, fluid leaves the capillaries and moves into the interstitial space, causing peripheral edema and potentially edema

in abdominal viscera/organs. If this occurs in the peritoneal cavity it is known as ascites. Liver congestion causes a decrease in hepatic function and a decrease breakdown of aldosterone causing further water retention.

Heart failure usually begins on the left side of the heart because the left ventricle is the main pumping chamber of the heart. When the left ventricle cannot contract enough, the ventricle is unable to push sufficient blood out of the heart; this is called systolic failure. When the left ventricle cannot relax enough, it cannot fill with enough blood; this is called diastolic failure [1].

Figure 1. Types of heart failure. Courtesy of http://www.heart.org.

Left-sided heart failureIn left ventricular failure, ventricular filling is reduced, and ventricular contractility is impaired, resulting in a decrease in cardiac output and

an increase in pressure in the pulmonary veins. This often results in pulmonary edema.

right-sided heart failureRight ventricular failure is usually a result of left-sided heart failure. When the left ventricle fails, blood is essentially pushed back into the lungs, resulting in back pressure and failure of the right ventricle.

When the right side of the heart fails or has decreased pumping power, blood backs up in the veins, resulting in swelling of the lower extremities/peripheral edema, the abdomen, and the liver/ascites [9].

Congestive heart failureA person can have a combination of both types of heart failure; this is known as congestive heart failure. The term “congestive heart failure” means that blood is backing up/congesting in the liver,

the abdomen, the lower limbs, and lungs. Not all heart failure is congestive, there can be symptoms of heart failure without blood backing up in the rest of the body [8].

Diagnosis and management of heart failureIt is important for the correct diagnosis to be made as soon as possible to prevent irreversible damage. The symptoms of cardiac failure are

often nonspecific, so a detailed history and clinical examination is necessary to exclude other possible causes.

the signs and symptoms of heart failure Patients with heart failure can report a number of symptoms including: Shortness of breath; difficulty breathing when lying down; swelling of the legs/abdomen; right-sided liver pain; yellowing of the skin and eyes; and weakness and/or fatigue [8].

Dyspnea, i.e. shortness of breath, is usually the first sign of heart failure. When the left ventricle is unable to eject sufficient blood into the systemic circulation, there is an increase in pressure in the left ventricle, which often leads to increased pressure in the pulmonary circulation, leading to pulmonary edema.

Nocturnal dyspnea occurs when a patient is supine, i.e. lying down. When supine, there is an increase in peripheral venous return from the extremities, and this leads to an increase in pressure in the left ventricle from an increase in blood return resulting in an increase in pressure back to the lungs because the heart is unable to eject sufficient blood into the systemic circulation.

Edema is an increase in fluid in the interstitial space as a result of congestion of the blood in the periphery, i.e. fluid seeps out of the blood vessels into the interstitial space. It occurs with both right and

congestive heart failure. Edema can occur in the ankles, the legs, the abdomen, the sacrum, and the scrotum.

Ascites are the accumulation of fluid in the abdomen as a result of right and congestive heart failure. Ascites can result in right hypochondrial or liver pain due to congestion of the liver. The liver becomes engorged with blood and liver function becomes impaired and bilirubin accumulates, leading to jaundice (i.e. yellow discoloration of the skin and conjunctivae). Although patients with heart failure may present with an increase in weight from the accumulation of fluid, some patients with severe heart failure and intestinal edema are unable to absorb food adequately, resulting in malabsorption and anorexia. Very often, patients with ascites have no appetite and feel nauseous and this can result in muscle wasting. Many patients with heart failure present with fatigue and lethargy which can be the result of dyspnea, muscle wasting, and/or malabsorption. Patients with heart failure often struggle to sleep at night because of nocturnal dyspnea. Reduced oxygenation of the brain can lead to altered mental states or confusion [7].


Clinical examination of heart failureThe clinical signs of heart failure depend on the cause, i.e. right sided heart failure, left sided heart failure, or both [7].

Right-sided heart failure: The clinical signs of right-sided heart failure include: Non-tender pitting edema in the feet/ankles; abdominal swelling with or without ascites; liver enlargement with tenderness; and or a visible jugular venous pulse. Severe right-sided heart failure can result in generalized edema or anasarca. Cardiac findings upon palpation of the heart may show right ventricular enlargement.

Auscultation may reveal a murmur of tricuspid regurgitation or incompetence.

Left-sided heart failure: The clinical signs of left-sided heart failure include shortness of breath/dyspnea, cyanosis, and hypotension. Palpation of the heart may reveal a displaced apical heartbeat, and auscultation may reveal a third and/or fourth heart sound. Pulmonary investigation may reveal crackling sounds at the base of the lungs, and in the case of a pleural effusion, dullness to percussion and decreased breath sounds at the bases of the lungs.

tests used in the diagnosis of heart failure[8]

Routine blood tests: Routine blood tests for cardiac failure diagnosis include: A metabolic panel including urea and electrolytes; a full blood count; liver function tests; thyroid function tests; a glucose level test; and a complete lipid profile.

Specialized blood tests: Serum natriuretic peptide (SNP): This is a hormone secreted by the heart as a result of increased ventricular stretch and it is considered a useful marker in the diagnosis of cardiac failure.

Other diagnostic tests: ● A 12-lead ECG can show evidence of ventricular hypertrophy/

enlargement, cardiac disease, and associated arrhythmias such as atrial fibrillation.

● A chest x-ray can show enlargement of the heart i.e. cardiomegaly, pulmonary congestion, and respiratory disease.

● Respiratory function tests are used to exclude respiratory causes of the above-mentioned symptom and signs.

● Echocardiography is considered the gold standard for diagnosing cardiac failure, as it provides information on the underlying structure of the heart and the amount of dysfunction. It can also be used to exclude other causes.

management of heart failureManagement of cardiac failure requires pharmacologic and non-pharmacological interventions [8]. Note that many of these drugs are used in other cardiac conditions and learning them now will allow for ease of learning later in the module.

Figure 2. Pharmacologic treatment of cardiac failure. From: http://study.com/academy/lesson/what-are-diuretics-definition-types-side-effects-examples.html.

Pharmacologic treatment of heart failure [14]

Diuretics are the drug of choices as a first line treatment of heart failure. Diuretics keep fluid from accumulating in the body and increase urination [11]. There are three types of diuretics used to treat heart failure:

● Loop diuretics. ● Thiazide diuretics. ● Potassium sparing diuretics.

Loop diuretics: Loop diuretics (e.g. furosemide) work in the Loop of Henle by increasing sodium and water secretion, and in the distal tubule of the kidney by increasing potassium secretion [11,14]. If using furosemide intravenously, it should be given slowly, as rapid infusion can lead to tinnitus and deafness. The most important side effects to monitor in this situation are hypokalemia and dehydration. Thus it is important to monitor serum urea (i.e. increased in dehydration) and electrolyte panels (i.e. K levels). Hypokalemia (low K) can be managed by switching to potassium sparing diuretics or using potassium supplements. Hypokalemia can cause cardiac arrhythmias and can be fatal.

Thiazide diuretics: Thiazide diuretics work in the distal tubule by inhibiting sodium and chloride reabsorption, resulting in an increased secretion of sodium and chloride by the kidneys [11,14]. Thiazide diuretics are usually given in combination with loop diuretics. The main side effect is hypokalemia, thus urea and potassium levels need to be monitored. Side effects of thiazide diuretics include hypotension (i.e. low blood pressure), headaches, and dizziness.

Potassium sparing diuretics/aldosterone antagonists: Potassium sparing diuretics (e.g. spironolactone, amiloride) work in the distal tubule of the kidney by increasing sodium and chloride secretion [11,14]. This group of drugs causes the retention of potassium, and is weaker than the diuretics already described. These are usually combined with either loop or thiazide diuretics. The most common side effects include hyperkalemia, dehydration, hypotension, and gastrointestinal upset.

Beta-blockers, e.g. atenolol, metoprolol: Beta-blockers slow the heart rate and reduce blood pressure [11,12]. Beta-blockers were once contraindicated in patients with heart failure, but medical trials have shown them to be effective for the treatment of heart failure; in fact,


beta-blockers often decrease mortality. When combined with diuretics and ACE inhibitors, beta-blockers improve the signs and symptoms of left-sided heart failure. Beta blockers decrease heart rate, so care should be taken when they are administered because they can lead to bradycardia, conduction disorders, fatigue, and bronchospasm, especially in patients with a history of asthma. The most common side effects of beta blockers include fatigue, cold hands, headache, gastrointestinal upset, and dizziness [12]. Precautions of beta-blockers include: They should not be used in people with asthma as they may trigger bronchospasm; in patients with diabetes, they may block signs of low blood sugar; and they can cause an increase in triglycerides. Beta blockers should not be stopped suddenly because of an increased risk of heart attack.

Angiotensin-converting enzyme drugs (ACE inhibitors), e.g. enalapril, lisinopril, or captopril: Ace inhibitors are a type of vasodilator, i.e. they relax blood vessels to lower blood pressure, resulting in an increase in blood flow and a decrease in workload on the heart [11,14,23]. ACE inhibitors are used in chronic heart failure cases as they work on the renin-angiotensinaldosterone system. Normally, renin is released from the kidneys when there is a decrease in kidney perfusion, stimulating angiotensin I to be converted to angiotensin II in the liver. Angiotensin II is a potent vasoconstrictor and also causes the release of aldosterone from the pituitary gland in the brain. Aldosterone causes the retention of sodium and water which in return increases blood pressure to maintain perfusion of the organs.

Ace inhibitors act by inhibiting angiotensin II as well as aldosterone release by the pituitary; there is no increase in sodium and water retention by the kidneys and blood pressure is lowered. ACE inhibitors also lead to an increase in bradykinin (i.e. a vasodilator) which can be responsible for some of the side effects of ACE inhibitors including dry cough, hypotension, and angioedema. ACE inhibitors

can cause a sudden decrease in blood pressure, and as a result, a small test dose is usually administered first. Precautions regarding ACE inhibitors include a decrease in the effectiveness of non-steroidal anti-inflammatory drugs. They should not be used in pregnancy because of the risk of birth defects. ACE inhibitors are contraindicated in patients with aortic stenosis [8].

Positive inotropes, e.g. dopamine, dobutamine:[14] Drugs which increase cardiac contractility are known as positive inotropes. They act by increasing the sympathetic nervous system stimulation. Dopamine is normally produced in the adrenal medulla and the brain. Dopamine acts on the heart, leading to an increase in cardiac contractility, and on the kidney, causing an increase in renal perfusion and an increase in urine output. Dopamine needs to be given by a central venous catheter because it causes necrosis (i.e. damage) to the surrounding tissues if any extravasation (i.e. leakage) occurs. The main side effects of dopamine are tachycardia, hypertension, arrhythmias, headaches, nausea, and vomiting. Patients need to be monitored closely and require initial and hourly observation of vital signs. Dopamine can also lead to vasoconstriction [8].

Cardiac glycosides digoxin, e.g. digitalis: Digoxin works directly on cardiac muscle; it slows down heart rate and increases the force of contraction. This leads to improved circulation and reduced swelling of the extremities. It is more likely to be given to patients with cardiac arrhythmias and/or when cardiac failure is worsening despite pharmacological treatment [11]. Several conditions lead to digoxin toxicity including hypercalcemia, hypokalemia, hypomagnesemia, and kidney disease [13]. Anticoagulants are prescribed for heart failure patients with atrial fibrillation, or sinus rhythm with a history of thromboembolism, left ventricular aneurysm or intracardiac thrombus[8].

non-pharmacologic treatment of cardiac failure Although pharmacologic treatment is the first line of treatment, non-pharmacologic treatments improve long-term prognosis. These consist of education, lifestyle advice, and exercise [8].

Nursing care:[58] Vital signs are directly affected by both right and left sided cardiac failure including:

● Pulse rate and rhythm: The pulse rate is often increased as a result of compensatory mechanisms for hypoxia and low cardiac output. Patients can have arrhythmias, indicating a poor cardiac output from a failing heart.

● Blood pressure: Blood pressure is likely to be abnormal, evidencing a low systemic blood pressure. The diastolic blood pressure can be abnormally elevated and this is indicative of congestion as a result of decreased blood return to the heart and the resulting inability of the heart to pump sufficient blood into the systemic circulation.

● Oxygen saturation: The percentage oxygen saturation is often decreased as a result of circulatory congestion and a causes a low oxygen saturation rate.

● Respiration: Respiratory rate is often increased due to hypoxia, but it is usually shallow because of general fatigue.

● Body temperature: Low levels of oxygenation of the body, i.e. hypoxia, lead to a lower metabolic rate and a lower body temperature. Providing oxygen and keeping the patient warm and on bed rest is an important component for treating cardiac failure.

● Lifestyle modification: The patient should be advised to: Acutely reduce activity to decrease the workload of the heart; stop smoking; and abstain from drinking alcohol.

● Dietary modification: The patient should be on a low-salt and a low-fat diet. A salt-free diet decreases the incidence of fluid retention and a low fat diet minimizes the risk for ischemic heart disease. Small meals are recommended to decrease the work of the heart.

● Weight needs to be assessed. ● Medication and oxygen therapy should be assessed. ● Digitalis/digoxin is commonly prescribed to increase the

contractility of the heart and therefore improve cardiac output. ● Diuretics are used to enhance the elimination of excessive fluid

from the body and decrease pulmonary and peripheral edema. ● Angiotensin converting enzyme inhibitors: ACE inhibitors

decrease aldosterone production, resulting in a decrease in the reabsorption of sodium and water.

Complications of heart failureThe complications of heart failure include organ damage (i.e. kidneys, liver, spleen, and/or brain) and heart valve problems (e.g. if the heart is enlarged).

the non-pumping diseases of the heartThis section will cover the non-pumping problems of the cardiovascular system including: Atherosclerosis/plaque; hypertension; coronary artery disease; peripheral artery disease; deep venous

thrombosis; valvular diseases of the heart; cardiac inflammation; myocardial ischemia; myocardial infarction; cardiomyopathies; rheumatic fever; and arrhythmias.


Atherosclerosis[15]

Atherosclerosis, i.e. the hardening of the medium and large arteries, is a condition in which plaque builds up on the artery walls. Plaque is made up of cholesterol, fatty substances, cellular waste, and fibrin (i.e. a clotting material in the blood). Risk factors for atherosclerosis and

plaque formation include: Elevated lipid levels; increasing age; family history of heart disease; high blood pressure; smoking; diabetes; and obesity [16]. Plaque accumulation in the walls of arteries can lead to partial or complete obstruction of arteries.

the pathogenesis of atherosclerosis[61]

Primary events causing atherosclerosis are repeated damage to the endothelial lining of the artery. The possible causes of damage to the wall of the artery include increased blood level lipids, high blood pressure, smoking, diabetes, and inflammation. Atherosclerosis begins when repeated injury to the artery wall mediates an inflammatory response, in turn causing white blood cells to adhere to the area of damage. These white blood cells transform into foam cells and collect cholesterol and cause the proliferation of smooth muscle cells in the wall of the artery. With time, these fat laden cells proliferate and build

up in the wall of the artery, causing patchy deposits, i.e. atheroma. Calcium is attracted to these atheromatous plaques and builds up, causing atherosclerosis, a “hardening” of the arteries.

The consequences of plaque formation are as follows: A piece of plaque can break away from the surface of the plaque; and/or a blood clot can form on the surface of the plaque. This can result in a cerebrovascular accident or a myocardial infarction. If this occurs in the periphery, it can result in gangrene [15].

types of lipids The two main types of lipids are triglycerides and cholesterol. Cholesterol is manufactured in the liver, and helps cells to function normally. Increased cholesterol is a result of consuming foods which are high in cholesterol. When a person eats an excessive amount of fats, excesses are stored in the liver as triglycerides. Elevated triglycerides are associated with an increased risk of atherosclerosis and often result in heart disease. There are no signs or symptoms of

atherosclerosis until the blood vessels become narrowed, therefore routine monitoring of blood lipid levels provides an early indication of potential problems. There are four different lipids which need to be monitored: Total cholesterol, triglycerides, HDL (high-density lipoprotein), and LDL (low-density lipoprotein). Although the mechanism is unknown, HDL is cardioprotective [17].

mAnAgement OF PAtIentS wItH eLevAteD BLOOD LIPID LeveLS

non-pharmacologic treatment of hyperlipidemiaFirst line management of elevated blood lipid levels involves lifestyle management with diet and exercise. When this does not help to reduce lipid levels, several drugs are used to treat hyperlipidemia. It is

important to note these drugs must have lifelong use after initiation of use [16].

Pharmacologic treatment of hyperlipidemia Lipid lowering drugs are also cardioprotective. There are different types of lipid lowering drugs, which are classified according to their mechanism of action. These mechanisms include: Bile acid binders; fibrin acid; niacin; cholesterol absorption inhibitors; omega-3 fatty acids; and statins [59].

Statins: Statins are the drug of choice for hyperlipidemia as they lower LDL cholesterol and decrease cardiac morbidity and mortality.

Statins inhibit hydroxymethylglutaryl CoA reductase, the main enzyme in cholesterol synthesis.

Desirable lipid levels in adults [59]: ● Total cholesterol: <200mg/dl. ● LDL cholesterol: <100mg/dl; if diabetic <70. ● HDL cholesterol: >40mg/dl. ● Triglycerides: <150mg/dl.

Hypertension (Ht)High blood pressure or HT is a disease which causes intermittent or a constant increase in blood pressure in the arteries. In the majority of cases, the cause is unknown; however, lifestyle factors have been

shown to play an important role in the development of hypertension [18].

Pathogenesis of hypertensionBlood pressure (BP) is defined as cardiac output (CO) multiplied by total peripheral resistance (TPR). Therefore, an increase in blood pressure is the result of an increase in cardiac output, or an increase in

total peripheral resistance, or both [62]. In most cases of hypertension or primary hypertension, cardiac output is normal or slightly increased and total peripheral resistance is increased.

risk factors of hypertension[18]

● Age: Men over 45; and women over 55 years of age. ● Race and ethnicity: Hypertension is increased in African

Americans. ● Family history: A family history of hypertension is increases the

risk of developing hypertension. ● Obesity: Obesity increases the risk of hypertension. ● Obstructive sleep apnea: This is present in a lot of patients with

hypertension.

● Lifestyle factors: These include smoking, a diet high in sodium, alcohol, sedentary habits, and stress.

● Additional risk factors: These include primary aldosteronism, renovascular disease, pheochrocytoma, Cushing’s syndrome, congenital adrenal hyperplasia, thyroid disorders, and drug induced or coarctation of the aorta [67].

Blood pressure is the force applied to the arteries as blood passes through them. Hypertension is the result of an increase in cardiac


output and/or an increase in total peripheral resistance [19]. Although the body can adapt to these changes in blood pressure, over time the heart may enlarge, i.e. hypertrophy, leading to a condition called cardiomyopathy. Cardiomyopathy is a major cause of heart failure. High blood pressure can lead to organ damage as well as damage to the peripheral arteries and arterioles.

There are two measurements used to determine high blood pressure: Systolic pressure (SBP) is the pressure measured when the heart

contracts and forces blood into the body; an elevated systolic blood pressure causes greater end organ damage and circulatory problems. Diastolic pressure (DBP) measures pressure in the arteries when the heart is at rest; an elevated diastolic pressure is a predictor of possible heart attack and stroke. A systolic blood pressure greater than 140 mmHg and/or a diastolic blood pressure greater than 90 mmHg indicates hypertension [68]. It is important to note that blood pressure fluctuates throughout the day and can be affected by exertion and stress.

types of hypertension[19]

1. Primary hypertension is also known as essential or idiopathic hypertension, where the cause is unknown. About 90% of all hypertension is primary and the causes are thought to be multifactorial and related to a host of lifestyle and genetic factors.

2. Secondary hypertension is caused by an underlying medical condition. The most frequent causes of secondary hypertension include kidney disorders, endocrine disorders, and certain medications.

Diagnosis of hypertension[19]

Symptoms: Hypertension is often known as the “silent” killer because there often are no reported symptoms until vital organs become damaged. Routine blood pressure monitoring during yearly physical examinations is therefore recommended. Blood pressure measurement is not very accurate or sensitive because it can be affected by a variety of factors including stress and exertion. Patients should not smoke, exercise, or consume caffeinated beverages prior to measurement. False low blood pressure readings are often the result of an arm cuff that is too wide and/or patient dehydration. False high blood pressure readings are often a result of a cuff that is too small and/or stress, caffeinated beverages, smoking, and recent exertion.

Blood pressure readings taken during office visits are often higher than normal. This is known as “white coat syndrome” and is a result of stress associated with a doctor visit, although BP readings can be normal when at home. Variations in BP readings cause the need for different types of monitoring which include: Ambulatory monitoring where an ambulatory BP monitoring device is worn for 24 hours; and home monitoring where the patient monitors BP at home as recommended by the American Heart Association.

Medical history: It is important to inquire regarding family and past medical history, especially as relates to hypertension, stroke, kidney disease, and diabetes as well as risk factors for hypertension which include a sedentary lifestyle, smoking, cholesterol levels, salt intake, diet, and medications.

Clinical examination: In patients with hypertension, there are often very little clinical findings upon clinical exam except for elevated blood pressure. It is important to determine pulse rate and look for distended neck veins, an enlarged thyroid, and/or an enlarged heart as well as murmurs, and the abdomen and leg pulses.

Tests: An electrocardiogram is routinely used in patients with hypertension. An exercise stress test is performed when a patient has symptoms of coronary artery disease. An echocardiogram may be ordered to determine if there is heart enlargement as a result of high blood pressure, incompetent valves, or heart failure. A Doppler ultrasound may be used to determine the perfusion of the kidneys and an ultrasound may be used to determine damage to the kidneys.

management of a patient with hypertensionThis includes pharmacological and non-pharmacological interventions. The non-pharmacological management includes lifestyle changes

addressing exercise, weight reduction, cessation of alcohol consumption, a low fat, low salt diet and cessation of smoking.

non-pharmacologic management of hypertension[22]

Dietary Considerations: ● Sodium: Lowering salt intake to less than 1,500mg per day is

highly beneficial to any patient with hypertension. ● Potassium: A diet rich in potassium (e.g. bananas, oranges, pears,

prunes, cantaloupes, tomatoes, dried peas, nuts, potatoes, or avocados) has been found to be beneficial in reducing hypertension provided there are no contraindications. Contraindications to increased potassium consumption include patients who have decreased kidney function, and patients who are taking medications which limit potassium excretion by the body (e.g. ACE inhibitors, digoxin, and/or potassium-sparing diuretics).

● Fiber: Increasing daily fiber can help to reduce hypertension.

● Omega-3 fatty acids: Some studies have found fatty acids helpful in keeping blood vessels more flexible.

● Calcium: Hypertension causes an increase in calcium loss by the body. Calcium regulates the tone of smooth muscles lining the blood vessels, and some studies have shown calcium to be beneficial in reducing hypertension.

Other considerations include: ● Sleep: Sleep apnea, along with any other chronic sleep disorder, is

associated with hypertension. ● Stress: Elevated stress levels are also associated with

hypertension.

Pharmacologic management of hypertension[22]

Diuretics: As discussed, diuretics help the kidneys eliminate excess salt and water. The three main types of diuretics include the thiazide diuretics, potassium-sparing diuretics and loop diuretics. The first-line drugs of choice for managing a patient with hypertension are the thiazide diuretics. roblems associated with diuretics: Loop and thiazide diuretics can lead to low potassium levels, or hypokalemia, which can result in arrhythmias and cardiac arrest. Potassium-sparing

drugs can lead to high potassium levels, or hyperkalemia, which can result in arrhythmias and difficulty in breathing. Thiazide diuretics can lead to erectile dysfunction and potentially gout [20]. Common diuretic side effects include fatigue, depression, irritability, urinary incontinence, dizziness, hypotension, and erectile dysfunction.

Beta blockers: The primary function of beta-blockers is to reduce the heart rate and to reduce blood pressure. They are usually used in


combination with other drugs such as ACE inhibitors and diuretics. Sudden cessation of beta-blocker therapy can cause a rebound increase in heart rate and blood pressure and can lead to angina and myocardial infarction. Problems associated with beta-blockers: Common beta-blocker side effects include fatigue, lethargy, vivid dreams, depression, memory loss, decreased exercise tolerance, dizziness, bradycardia and erectile dysfunction.

ACE inhibitors: The primary function of ACE inhibitors is vasodilation and therefore decreasing the workload of the heart. Patients with a previous history of cardiac disease are good candidates for this class of drug. ACE inhibitors are often combined with Aspirin and can be used safely in combination. Problems associated with ACE inhibitors: Common ACE inhibitor side effects include increased potassium retention by the kidneys leading to hyperkalemia, which can result in cardiac arrest; they can also result in dry cough and angioedema. ACE inhibitors SHOULD NOT be combined with potassium-sparing diuretics.

Angiotensin receptor blockers (ARB): Angiotensin receptor blockers are similar to ACE inhibitors in that they block the conversion of angiotensin I to angiotensin II and lead to enlargement of blood vessels

and as a result, decrease blood pressure. They have fewer side effects than ACE inhibitors (especially coughing) and are often prescribed as an alternative therapy. Common ARB side effects include low blood pressure, dizziness, hyperkalemia, drowsiness, and nasal congestion. They are contraindicated in pregnant women.

Calcium channel blockers: Calcium channel blockers prevent calcium from entering the heart and blood vessel walls, and lead to vasodilation. Calcium channel blockers also decrease heart rate, resulting in decreased blood pressure, relief of chest pain, and control of irregular heartbeat. Common calcium channel blocker side effects include peripheral edema, constipation, fatigue, gingivitis, erectile dysfunction, and potentially harmful interactions with grapefruit and oranges [21].

Alpha blockers: Alpha blockers cause vasodilation in the small blood vessels. They are generally not the first-line choice for hypertension, but are used in combination with other anti-hypertensive drugs.

One of the most difficult problems when treating patients with hypertension is a lack of compliance because hypertension causes minimal symptoms, and patients are often non-compliant.

Standard nursing protocol for primary hypertension in adults Primary hypertension with no underlying cause is defined as a systolic blood pressure greater or equal to 140mmHg, and a diastolic blood pressure of greater or equal to 90mmHg on at least two occasions.

Secondary hypertension has an underlying cause. More can be found at: http://millionhearts.hhs.gov/files/Hypertension-Protocol.pdf [22].

Complications of hypertensionThe most serious consequence of hypertension is damage to organs including the kidneys, eyes, and heart. Hypertension is the causative factor for 75% of strokes. Hypertension is the main causative agent for hypertensive heart disease. Hypertensive heart disease includes

coronary artery disease, heart failure, and cardiac arrhythmias. Organ damage includes stroke, diabetes, kidney disease, dementia, eye damage, and sexual dysfunction.

Coronary artery disease Coronary artery disease is also known as ischemic heart disease and is the result of atherosclerosis. The coronary arteries become hardened due to the calcification of the plaque in the walls of the blood vessels

leading to narrowing of the arteries and a reduced flow of blood. Atheromatous coronary arteries are more susceptible to injury, and clot formation which usually results in a heart attack.

Heart attackA heart attack is the result of one of two disease processes: Plaque develops fissures and tears, platelets adhere to the fissure or tear, and a blood clot forms which further decreases blood flow through the

arteries; or the artery becomes blocked as a result of plaque formation leading to decreased blood flow and ischemia of the heart tissues.

risk factors for coronary artery diseaseThe risk factors for coronary artery disease mirror the risk factors for all cardiac diseases and include age, gender (i.e. increased risk in males), genetic factors, family history, and race and ethnicity (i.e.

increased risk in African Americans). Lifestyle factors that increase risk include smoking, sedentary habits, poor diet, and obesity [23].

medical conditionsSeveral medical conditions are associated with increased risk of heart disease. Obesity and metabolic syndrome as well as excess body fat in the abdominal region are associated with increased risk

of cardiovascular disease as well as increased levels of low-density lipoprotein/LDL, hypertension, diabetes, peripheral artery disease, and depression.

Symptoms of coronary artery diseaseCommon symptoms of coronary artery disease include chest pain/angina, shortness of breath on exertion, and rapid heartbeat. In many cases, coronary artery disease is asymptomatic.

Angina is the chest pain felt as a result of lack of oxygen, or myocardial ischemia, to the heart tissue. There are two types of angina: Stable angina, which is predictable; and unstable angina, which is

unpredictable and is often more serious. The intensity of the pain from angina has no correlation to the amount of heart tissue damage [25].


Pathogenesis of coronary artery diseaseThe underlying pathology of coronary artery disease is atherosclerosis: As the atheromatous plaque grows it causes obstruction of the lumen of the coronary artery. In some cases, an atheromatous plaque can rupture, resulting in activation of platelets and a coagulation

cascade, causing thrombus formation that can lead to coronary artery obstruction, or acute coronary artery disease, or myocardial infarction[63].

Stable angina and chest painThe pain of stable angina is predictable, meaning it is usually triggered by certain events or activities, of which the patient is fully aware, e.g. exercise, cold weather, emotional stress, and large meals. Stable angina is usually relieved by rest and responds well to nitroglycerin. Angina

is not affected by breathing or change of position. The commonest time for stable angina to occur is between six AM and noon. A typical attack lasts minutes, but in the event of a much longer duration, the diagnosis of angina is usually excluded [26].

Symptoms of anginaChest pain experienced from angina has classic symptoms, and is often described as a crushing pressure in the chest. It is characteristically a dull pain which radiates to the neck, the jaw, the left shoulder, and arm. It is rarely described as a sharp stabbing pain. Other symptoms which may accompany angina include shortness of breath (SOB), nausea,

vomiting, cold sweats, indigestion, unexplained fatigue, dizziness, and palpitations. It is important to note that women usually experience atypical symptoms of angina which include abdominal discomfort, nausea, fatigue, and weakness as opposed to the typical chest pain.

unstable angina and acute coronary syndromeUnstable angina is potentially fatal and usually occurs when a coronary artery becomes blocked or occluded. Unstable angina occurs

just prior to a heart attack or infarct; it is usually sudden and without warning.

Other types of anginaPrinzmetal’s angina: This occurs with coronary artery spasm or vasospasm. It usually occurs at rest and often accompanied by arrhythmia. The pain is rapidly relieved by nitroglycerin.

Silent ischemia: People with silent ischemia have no pain during an angina attack, but these individuals have a higher incidence of serious morbidity and mortality because of the lack of the warning signs experienced with angina.

Other causes of chest painMuscular pain, arthritis, heartburn, and asthma as well as heart-related chest pain account for less than fifty percent of chest pain.

Diagnosis Tests used to diagnose the type of chest pain are dependent on the severity of the symptoms. The normal course of progression is to start with the simplest tests first [23].

routine non-invasive tests ● Electrocardiogram: An electrocardiogram (ECG) is the first-

line test for the diagnosis of myocardial ischemia even though 50% of patients have normal ECG findings in the presence of ischemia. An ECG is used for the diagnosis of most cases of heart disease [25]. The ECG measures the electrical activity of the heart and the various waves that are seen on the ECG correspond to the sequence of the cardiac cycle. The P wave occurs with atrial contraction, the QRS series corresponds to ventricular contraction, and the T wave occurs after ventricular contraction.

● The most important finding with myocardial ischemia is ST segment elevation and Q waves. These waves are indicative of coronary artery occlusion, but are not the only factors needed to make the diagnosis of myocardial ischemia.

● Exercise stress test: The exercise stress test is used to determine heart function during physical activity or increased workload on the heart [24]. It is used to diagnose coronary artery disease, and arrhythmias and is also used as a guide for the treatment of other heart diseases. The patient is connected to an ECG machine while exercising. The risks associated with an exercise stress test include low blood pressure, arrhythmias, and rarely, a myocardial infarction.

● Echocardiogram: The echocardiogram uses ultrasound to visualize the heart and is useful to determine if the heart muscle

has been damaged and the extent of the damage. Although it is much more expensive than an ECG, it is a valuable test for assessing the damage. A stress echocardiogram can also be used; this procedure is similar to an exercise stress test as it is performed on a treadmill or stationary bike and determines heart function via echocardiogram.

● Radionucleotide imaging: Radionucleotide procedures use imaging techniques to visualize radioactive elements in the various regions of the heart to determine damage. It is useful for diagnosing the severity of unstable angina and the severity of coronary artery disease as well as serving as an indicator to determine success rates for coronary artery surgery and diagnosing whether a myocardial infarction has occurred.

● Myocardial perfusion (blood flow) imaging test (thallium stress test): This test is used to determine blood flow to the heart muscle and is usually done in conjunction with an exercise stress test. It is a reliable indicator of severe heart events.

● Radionuclide angiography: This is a technique for visualizing the major blood vessels and chambers of the heart.

● Magnetic resonance angiography: This provides a three- dimensional view of the major arteries supplying the heart.

● Computed tomography (CT scan): CT scans can be used to visualize the coronary arteries.


● Calcium-scoring CT scan: This test is used to determine calcium deposition in the coronary arteries which normally occurs with plaque formation. A person with a low calcium score is unlikely to have coronary artery disease and vice versa.

● CT angiography: This test can be used to assess the coronary arteries, but it is not as reliable as angiography and therefore not a diagnostic test of choice.

Invasive tests ● Angiography: Is used to determine the exact anatomy or location

of disease in the coronary arteries by injecting radioactive dye into the coronary arteries via the arm or leg. An x-ray shows the flow of blood through the arteries.

● Treatment: Lifestyle changes are the first-line approach for the treatment of coronary artery disease, and are usually combined with medication [23].

There are a variety of medications used to treat coronary artery disease. These include anti-platelet and anticoagulant drugs, beta-blockers, ACE inhibitors, nitrates, and calcium channel blockers. Surgical intervention is indicated for people with unstable angina which does not respond to medical treatment, recurrent episodes of

angina which have a duration of longer than twenty minutes, acute coronary syndrome, and severe coronary artery disease.

The two main types of surgery for coronary artery disease are coronary artery bypass grafting (CABG) and percutaneous coronary intervention (PCI or angioplasty). With CABG, the surgeon creates a graft using a blood vessel from another part of the patient’s body to bypass coronary artery obstruction(s). CABG is an invasive procedure and is usually reserved for cases with multiple narrowed coronary arteries [25]. Angioplasty involves the placement of a catheter with a deflated balloon into the narrowest part of the coronary artery. The balloon is inflated to compress plaque deposits against the artery walls and improves blood flow [26]. The risks associated with CABG include bleeding, arrhythmias, infection of the chest wound, stroke, and myocardial infarction [27]. There are risks associated with angiography which include: Blood clots in the stent; re-obstruction of the coronary artery by plaque formation; and a small increase in the risk of myocardial infarction, stroke, and life threatening bleeding. Coronary artery surgery does not cure coronary artery disease and it is of utmost importance to adopt a healthy lifestyle by decreasing obesity, following a low-fat diet, and exercising as well as smoking and alcohol cessation [23].

meDICAtIOnS uSeD tO treAt COrOnAry Artery DISeASe[23,26]

Anti-platelet and anticoagulant drugs: The normal blood clotting mechanism is a cascade of events triggered by injury to the blood vessels; this sets up an inflammatory response whereby chemical signals trigger the platelets to accumulate at the site of injury. Once the platelets arrive at the site of injury, they aggregate and clump at the wound and release thromboxane. Thromboxane is the enzyme necessary to facilitate clotting of the blood, and it acts to allow prothrombin to be converted into thrombin. In turn, thrombin acts to allow fibrinogen to be converted to fibrin resulting in blood clot formation.

Both anti-platelet and anticoagulant drugs prevent the formation of blood clots, but they have different mechanisms of action. Anti-platelet drugs prohibit platelets from sticking together and prevent the formation of blood clots. Anticoagulant drugs are blood thinners prohibit blood from clotting and prevent blood clot formation. In patients with coronary artery disease, anti-platelet drugs are the drug of choice whereas anticoagulants are used for patients with atrial fibrillation or a heart valve prosthesis.

It is important to note: A thrombus is a blood clot that forms in a blood vessel and stays in situ (in position), and an embolus is a blood clot that dislodges from its primary position and travels to another location in the body. Both thrombi and emboli can lead to occlusion and deprive the local tissues of oxygen. In the heart this is equivalent to a myocardial infarction.

Aspirin: Is a non-steroidal anti-inflammatory (NSAID); it prohibits platelets from sticking together and prevents blood clot formation[28]. Aspirin inhibits the production of thromboxane in the clotting mechanism, and without the release of thromboxane, platelets will not stick together. Aspirin helps in the prevention of myocardial infarction and stroke. It is important to note that long term use of aspirin can lead to the same side effects as long-term use of any NSAID and increase the risk of bleeding from the stomach. A daily dose of 75-81mg is usually the drug of choice for preventing heart disease and stroke in patients with no prior history of heart disease or stroke.

Other anti-platelet drugs: ● Clopidogrel (Plavix): Works to inhibit the production of

thromboxane. This is the standard treatment for acute coronary syndrome and is used in patients who are allergic or cannot tolerate aspirin.

● Beta-blockers: Can also be used to treat coronary artery disease as they reduce the workload on the heart by slowing heart rate

and decreasing blood pressure [11,12]. Beta-blockers are used in the majority of patients who have had a myocardial infarction or acute coronary syndrome, and they are also the drug of choice for older patients with stable angina and silent ischemia. A nasal form of propranolol can be used to prevent exercise-induced angina. The side effects of beta blockers have already been discussed, but it is important to note that beta blockers can reduce HDL, the cardio-protective lipoprotein, and they should not be used in patients with asthmas, emphysema, or chronic bronchitis. Patients should never suddenly discontinue beta blockers as this can lead to a rebound increase in heart rate and blood pressure.

● Angiotensin converting enzyme: ACE inhibitors are important cardio-protective drugs, especially in patients with hypertension, diabetes, and left-sided heart failure [11,23]. The mechanism of action and side effects have been discussed earlier, but it is important to note that the commonest side effect of ACE inhibitors is an irritating cough. Other important side effects include hyperkalemia, allergic reactions, excessive decrease in blood pressure, and angioedema.

Nitrates: Nitrates release nitric acid which relaxes the smooth muscle of the vascular walls, leading to vasodilation and reducing oxygen demand of the heart by improving blood flow [23]. Nitrates can be absorbed by the gastrointestinal tract, or the skin as well as sublingually and bucally, e.g. pocketed between the upper lip and the gums.

Rapid acting nitrates: These are used for the treatment of acute episodes of angina. The recommended treatment protocol for rapidly acting nitrates is: At the onset of an attack the patient takes one tablet; if the pain is not relieved after five minutes, a patient can take another every five minutes; if after three doses the pain does not subside, the patient should go to the emergency room as soon as possible. Nitroglycerin is an unstable compound and certain precautions should be taken when storing this drug including: Not keeping more than 100 tablets in the original container; discarding the cotton filler; and keeping the container in a cool dark place and closed.

Intermediate and long acting: These have a slower onset of action and are often used to prevent exercise-induced angina. Long-acting nitrates often lose their effectiveness over time, and as a result, patients are prescribed “nitrate breaks” to prevent tolerance.

Side effects of nitrates: Common side effects include headaches, dizziness, nausea and vomiting, blurred vision, fast heartbeat,


sweating, and flushing of the face and neck. Low blood pressure and dizziness can be relieved by lying down with the legs elevated. Side effects are made worse by alcohol, beta-blockers, calcium channel blockers, and antidepressants. Patients taking nitrates cannot take medication for erectile dysfunction as these drugs, when combined, cause a decrease in systemic blood pressure and coronary blood flow, which can be fatal. Other serious side effects include fever, joint or chest pain, sore throat, skin rash, abnormal bleeding or bruising, weight gain, and swelling of the ankles. Withdrawal from nitrates should be done slowly to prevent rebound angina.

Calcium channel blockers: Calcium channel blockers work to reduce the heart rate, dilate coronary blood vessels, and improve the oxygen supply and decrease the oxygen demands of the heart [21,23]. They also decrease blood pressure. Calcium channel blockers have varied efficacy and are often used in patients who cannot tolerate beta blockers. However, there is no strong evidence that the use of calcium channel blockers improves survival rates. Long-acting calcium channel blockers may be beneficial to patients with angina. Best results are obtained when combining calcium channel blockers with other drugs for the treatment of angina. Short acting calcium channel blockers are contraindicated for the treatment of stable or unstable angina and can have serious side effects, including sudden cardiac death.

Peripheral artery diseasePeripheral artery disease is similar to coronary artery disease and is caused by the narrowing of the peripheral arteries supplying oxygen to the legs, stomach, arms, and head; it most commonly affects the legs. Both coronary and peripheral artery disease are caused by the buildup

of fatty deposits on the wall of the arteries, leading to artery narrowing and decreased oxygen supply [29]. With peripheral artery disease, the extremities do not have adequate blood flow and oxygen supply, causing pain on walking, i.e. claudication [30].

Symptoms of peripheral artery diseaseMany people with peripheral artery disease do not have any symptoms, but some patients experience claudication. Claudication ranges from mild discomfort to debilitating pain, and is characterized by cramping in the muscles of the hip, thigh, and calf. It is often aggravated by climbing stairs. It can even occur during rest, causing sleep disturbances. Claudication can be relieved temporarily by hanging

the leg off the side of the bed, or gentle walking. Other symptoms of peripheral artery disease include: Leg numbness and/or weakness; lesions of the foot, heel, and toes which do not heal; coldness of the lower legs; a change in color or loss of hair; slower growth of toenails; shiny skin; an absent pulse; and erectile dysfunction.

etiology of peripheral artery diseaseThe commonest cause of peripheral artery disease is plaque formation or atherosclerosis of the peripheral arteries, but it can also be a result of injury, blood vessel inflammation, anatomical deviation, and

radiation exposure. The risk factors for peripheral artery disease are the same as that of coronary artery disease.

Complications of peripheral artery disease[30] Critical limb ischemia: Decreased blood supply to the extremities, combined with injury and infection can result in death of the surrounding tissue and/or gangrene, leading to amputation.

Stroke and myocardial infarction: Atherosclerosis from peripheral artery disease usually occurs in other blood vessels, especially the heart and the brain, and can lead to myocardial infarction and stroke.

Diagnosis of peripheral artery disease[30]

Signs of peripheral artery disease: An absent or weak pulse may be found on clinical examination, evidence of poor wound healing, decreased blood pressure in the affected limb and bruits may be heard on auscultation.

Tests used for the diagnosis of peripheral artery disease: ● Ankle brachial index: This compares blood pressure readings of

the upper and lower extremities.

● Ultrasound: Doppler ultrasound can identify blocked or narrow blood vessels and can be used to evaluate the severity of the condition.

● Angiography: This allows for visualization of blood flow through the narrowed blood vessels using x-ray imaging or computerized tomography angiography (CTA). Catheter angiography is a far more invasive procedure, but allows for simultaneous dilation of the narrowed artery.

● Blood tests: Cholesterol, triglycerides, CMP and blood sugar levels need to be investigated.

treatment of peripheral artery disease There are two main goals for the treatment of peripheral artery disease: (1) to manage symptoms to allow for physical activity; and (2) to stop the progression of atherosclerosis and reduce the incidence of myocardial infarction, gangrene, and stroke [30]. The non-medical treatment of peripheral artery disease incorporates lifestyle changes discussed earlier, and cholesterol lowering medications to reduce plaque formation.

Cholesterol-lowering medication/statins: Statins work to reduce the amount of cholesterol synthesized by the body by blocking an enzyme called HMG CoA reductase. Due to this cholesterol cannot be synthesized [31]. Statins are known as HMG CoA reductase inhibitors and may also help with cholesterol reabsorption from plaque buildup

within arteries [32]. One of the biggest problems with statins is their discontinuation because of intolerable side effects.

Side effects:[33] Muscle pain can vary from mild to severe, and in rare cases result in rhabdomyolysis, life-threatening muscle damage. Statins can lead to inflammation of the liver so monitoring of liver function is important. They can cause an elevation in serum glucose levels and can cause or worsen Type-II diabetes. Statins have been associated with memory loss and confusion. The risk of developing side effects from statins is increased by taking multiple medications for the treatment of elevated cholesterol. Other risk factors include smaller body frame, age over 65 years of age, kidney or liver disease, and excessive alcohol consumption.


Certain foods and drugs interact with statin metabolism. Grapefruit interferes with the breakdown of statins in the gastrointestinal tract. Certain drugs may interact with statins leading to an increased incidence of side effects, e.g. amiodorone which is used for the treatment of arrhythmias, other cholesterol-lowering drugs, protease inhibitors, antifungals and immunosuppressants. Other medications include hypertension medication, blood sugar medication, and anti-platelet medication.

Medication to reduce the symptoms of peripheral artery disease: Cilostazol has a dual function of increasing blood flow to the limbs by vasodilation and it also acts as a blood thinner. It is used primarily to

decrease the symptoms of claudication. The commonest side effects include headache and episodes of diarrhea.

Angioplasty and surgery: The treatment of peripheral artery disease is similar to treatments used for coronary artery disease. Angioplasty stretches the artery open to reduce obstruction to blood flow, and a stent may be left in place. Bypass surgery allows blood to be diverted around the obstruction.

Thrombolytic therapy: A thrombolytic/clot-dissolving agent can be injected into the affected artery in an attempt to dissolve a blood clot. A supervised exercise program improves the symptoms of peripheral artery disease.

Deep venous thrombosis (Dvt) In DVT, a blood clot forms in a vein deep within the body [34]. It primarily affects large veins of the leg and thigh, but can even occur in the veins of the arms. Deep venous thrombosis is most common after the age of 60, but it can occur at any age. There are several factors which increase the risk of a DVT, including: Bed rest or sitting in one position for a long period of time, e.g. a long trip on a plane; family history of blood clots; fractures of the pelvis or legs; postpartum or

pregnancy; obesity; recent surgery causing immobility; an increased production of red blood cells by the bone marrow, i.e. polycythemia; a longterm blood vessel catheter; and/or post procedure–pacemaker catheter. There are also several conditions which increase the risk of DVT including cancer, certain autoimmune disorders, smoking, and oral contraceptives.

Pathophysiology of deep venous thrombosisIn the lower extremities, DVT is the result of impaired venous return. This occurs in cases of immobilization, and in patients that are post-surgery, obese, or have taken long trips [64]. Other

causes include endothelial injury following trauma or fractures and hypercoagulability.

Clinical signs and symptoms of deep venous thrombosisA blood clot can cause changes in skin color, and skin that is warm to the touch as well as leg swelling and pain. A warm, red, swollen leg which is tender to the touch is the classic sign of a DVT.

Tests to diagnose a DVT:[35]

● Doppler ultrasound: Is used to determine the presence/absence of a blood clot.

● D-dimer blood test: Is a blood test used to measure a substance that is released when a blood clot breaks up.

● Blood tests: Several blood tests are required to determine the presence of increased blood clotting, including active protein-c and-s, anti-thrombin levels, antiphospholipid antibodies, complete blood count, and lupus anticoagulant.

treatment of deep venous thrombosisThe treatment of DVT involves the use of anticoagulants. Heparin is usually the drug of choice. Heparin prevents the formation of new blood clots and prevents old clots from enlarging. A blood thinning drug, e.g. Warfarin, is usually started at the same time as Heparin, and

when warfarin levels are at the correct level, Heparin is discontinued. Warfarin causes increased bleeding even when levels are adjusted correctly. Pressure stockings are also prescribed to improve blood flow and reduce the incidence of complications.

Long-term complications of DvtPain and skin color changes are common side effects of DVT. Some patients will have long-term pain and swelling and this is known as post-phlebitic syndrome. Blood clots from the legs can travel to the

lungs (i.e. pulmonary embolus) and even the brain (i.e. cerebrovascular accident).

Overview of anticoagulantsAnticoagulants are reserved for the treatment of life-threatening diseases, these include myocardial infarction, pulmonary embolism, disseminated intravascular coagulation/DIC, and deep vein thrombosis[35]. The therapeutic window for clot dissolution is approximately six hours. Anticoagulants consist of a variety of different drugs which fall into different classes and have different mechanisms of action, routes of administration and side effects:

● Fibrinolytic agents, e.g. Streptokinase, degrade fibrinogen and their primary action is to eliminate formed blood clots.

● Anticoagulants, e.g. heparin and warfarin, inhibit the clotting cascade and prevent the formation of a thrombus. It is important to note that Warfarin has a narrow therapeutic index: It is 99% bound

to plasma albumin; it is eliminated by the liver (via cytochrome P450); and it is the prototype of drug-drug interactions. Warfarin is completely contraindicated in pregnancy. Certain drugs always interact with Warfarin, aspirin, cimetidine and phenytoin. Alcohol interferes with the metabolism of Warfarin by interacting with cytochrome P450.

● The anti-platelet drugs, e.g. Acetylsalicylic acid, interfere with platelet adhesion or aggregation and they are used for the prevention of initial blood clot formation.


Cerebrovascular accident (stroke or CvA)A cerebrovascular accident occurs when areas of the brain are deprived of blood and oxygen, leading to cell death [36].

Types of cerebrovascular accident: ● Ischemic: An ischemic stroke occurs when there is obstruction

to brain blood flow. The majority of strokes are ischemic. A thrombotic stroke occurs when plaque builds up in the artery wall, leading to obstruction of blood flow, or when a blood clot (i.e. embolus) dislodges from an artery wall in the periphery of the body and is swept towards the brain where it becomes lodged in a narrower brain artery. An ischemic stroke from an embolus is a complication of deep venous thrombosis. A transient ischemic attack (TIA) is also the result of an embolism but in these cases, the symptoms are transient and usually disappear within twenty-four hours. TIAs are often precursors for a larger stroke.

● Hemorrhagic: A hemorrhagic stroke occurs when a blood vessel supplying the brain bursts or leaks. Hemorrhagic strokes can occur with uncontrolled hypertension or from overtreatment with

anticoagulants. Congenital abnormalities such as arteriovenous malformations (i.e. an abnormal tangle of thin-walled blood vessels) can rupture without warning. Types of hemorrhagic stroke include intracerebral hemorrhage, where blood leaks out of the blood vessel into the surrounding brain tissue. Brain cells around the leak are deprived of oxygen, leading to cell death. The most common causes of intracerebral hemorrhage are high blood pressure, trauma to the head, vascular abnormalities, and overtreatment with blood thinners. A subarachnoid hemorrhage occurs when an artery close to the surface of the brain bursts and leaks into the space between the skull and the surface of the brain. This is signaled by a sudden incapacitating headache. A subarachnoid hemorrhage is caused by the rupture of an aneurysm; an aneurysm is a small pouch on the surface of a blood vessel. After this kind of rupture, blood vessels supplying the brain erratically vasodilate and vasoconstrict, leading to further damage. Risk factors for a CVA are the same as those for coronary artery disease.

Complications of strokeA stroke can lead to temporary or permanent disability and the complications are related to the length of time the affected area is deprived of oxygen [36]. The complications include paralysis, difficulty talking/swallowing, memory loss, aptitude, loss of vision, and emotional problems. Pain from paralysis, decreased mobility and

muscular contraction is an ongoing complication following a stroke and central pain syndrome where a person may be super-sensitive to temperature and touch is known as central pain syndrome. Central pain syndrome is difficult to manage because the origin of the pain is from within the brain.

Pulmonary embolusThe most common cause of a pulmonary embolus is a blood clot that dislodges from a DVT of the legs or pelvis [37]. The blood clot breaks off from the DVT and travels (i.e. embolus) to the lungs where it becomes trapped in the blood vessels of the pulmonary system. Less frequent causes of a pulmonary emboli are the same as causes for

DVTs and include air bubbles, fat droplets, amniotic fluid, parasites, and tumor cells. Certain disorders lead to an increased incidence of a pulmonary embolus, including diseases of the immune system, cancers, and inherited disorders affecting blood clotting.

Pathogenesis of a pulmonary embolus[65]

As a consequence of DVT, a clot can break free and travel in the venous system to the right side of the heart and then lodge in the lungs, causing a partial or complete obstruction of a pulmonary artery. The consequences of a pulmonary embolus depend on the size of the

embolus as well as the functioning of the lungs and the right ventricle. A small embolus may have no consequences while a large embolus may cause mortality. A saddle embolus occurs at the bifurcation of the right and left pulmonary arteries; saddle emboli are usually fatal.

Symptoms of pulmonary embolusThe predominant symptom of pulmonary embolism is chest pain that occurs under the sternum or on one side of the chest. The pain characteristics vary from sharp or stabbing pain to burning or aching heavy pain. Pain from a pulmonary embolus is usually made worse by deep breathing and a patient may bend over or hold their chest in

response to pain. Other symptoms include bluish discoloration of the skin, dizziness, fast heart rate, wheezing, anxiety, leg pain, and low blood pressure as well as episodes of coughing and blood-stained mucus, sudden shortness of breath, and clammy skin.

Signs of pulmonary embolusClinical signs of a pulmonary embolus include a distressed patient with evidence of cyanosis (i.e. bluish clammy skin), rapid respiration or wheezing, tachycardia (i.e. rapid heart rate), and hypotension.

tests used for the diagnosis of a pulmonary embolusArterial blood gasses measure oxygen, carbon dioxide, and acidity levels of the blood to determine how well the lungs are functioning. Pulse oximetry can also be used to measure oxygen levels, but it is not as accurate as an arterial blood gas measurement. Blood tests are usually done to determine the possibility of conditions causing an

increased incidence of blood clots. Imaging tests are used to determine the location of a blood clot. These include chest x-ray, chest CT angiogram, a ventilation-perfusion scan (VQ scan), and a pulmonary angiogram. Other tests include a chest CT scan, d-dimer blood test, Doppler ultrasound of the legs, and echocardiogram.

treatment of pulmonary embolusA pulmonary embolism is a life-threatening condition. Treatment involves the use of anticoagulants to thin the blood, and thrombolytics

to dissolve blood clot(s). The prognosis of pulmonary embolus is dependent on the underlying cause.


Inflammation of the heart or carditisInflammatory diseases of the heart are named according to the layer of the heart affected. Inflammation of the endocardium is known as endocarditis. Inflammation of the myocardium is known as myocarditis, and inflammation of the pericardium is known as

pericarditis. Inflammation of all the layers of the heart is known as pancarditis, and this occurs with rheumatic fever and rheumatic heart disease.

rheumatic fever[38]

Rheumatic fever is an inflammatory heart disease that is a complication of inadequately treated strep throat or scarlet fever, caused by type-A beta-hemolytic streptococcus spp. bacteria. The disease involves inflammation of all the layers of the heart (i.e. pancarditis) during the acute phase. The chronic form of the disease

is known as rheumatic heart disease. The disease occurs most frequently in children from five to fifteen years of age. The incidence of rheumatic fever in the United States (U.S.) is decreasing due to the use of antibiotics.

risk factors for rheumatic fever[39]

Rick factors for rheumatic fever include a family history of the condition, immunodeficiency, infection with Type A streptococcus

bacteria, and environmental factors including overcrowded living conditions, poor sanitation, and malnutrition.

Pathogenesis of rheumatic fever[40,41]

Group A beta-hemolytic Streptococcus spp. bacteria cause an antibody-mediated Type-II hypersensitivity reaction. In this autoimmune event, the immune attacks the tissues of the heart, skin, and the central nervous system, causing inflammation. As the disease becomes chronic, fibrous scarring replaces the inflammation and causes damage to the valves of the heart. The mitral valve is most

commonly affected. The valve leaflets become scarred and shortened, leading to either stenosis of the mitral valve or incompetence of the mitral valve. Stenosis is when the valve leaflets become rigid and deformed and often fused together, obstructing blood flow. Incompetence or regurgitation occurs when the valve fails to close, allowing for backward flow of blood.

Clinical manifestations of rheumatic fever[41]

The clinical manifestations of rheumatic fever affect several systems in the body. In the joints there is synovial inflammation but no chronic or residual scarring occurs. Upon biopsy, Aschoff bodies are found; these are granulomas which consist of leukocytes, monocytes, and interstitial collagen. In the skin, subcutaneous nodules (i.e. small lumps) under the surface of the skin occur and these are also characterized by aschoff bodies during biopsy. The skin manifestations include areas of erythema marginatum on the trunk and limbs [69]. The

CNS manifestations of rheumatic fever include sydenham chorea; this is characterized by personality changes, muscle weakness, and involuntary movements of the body. Erythema marginatum and sydenham chorea are characteristic signs of acute rheumatic fever [69]. The cardiac manifestations of acute Rheumatic Fever include mitral regurgitation, pericarditis, and potentially, aortic regurgitation. In chronic rheumatic heart disease, there is evidence of mitral stenosis and aortic regurgitation.

the clinical symptoms and signs of rheumatic fever[41]

The symptoms of rheumatic fever typically occur two to three weeks after an untreated streptococcal infection:

● Joints: Patients often complain of painful and tender joints, and the pain characteristically migrates from joint to joint and is known as a migratory polyarthritis. This is usually accompanied with fever. The smaller joints are frequently involved, but the pain can affect the ankles, knees, hands, and feet.

● The skin: Subcutaneous nodules occur on the extensor surface of the large joints; this usually occurs in combination with arthritis and carditis.

● Erythema marginatum: A flat or slightly raised painless rash that usually occurs on the trunk and extremities but not on the face. The edges of these macules and/or papules are raised and the centers are clear.

● Sydenham chorea: Consists of rapid irregular jerking movements which can be precipitated by laughing or crying. This usually begins in the hands and becomes generalized to include the feet and face.

● The heart: Patients complain of high fever, chest pain and rapid heart rate/tachycardia. The clinical findings include a pericardial rub, cardiac enlargement and heart failure. Although all the layers of the heart are involved the most common clinical finding is inflammation of the valves of the heart; this is diagnosed by auscultation and the finding of murmurs especially of the mitral and aortic valves. The clinical manifestations of heart failure may also occur.

Diagnosis of rheumatic feverThe diagnosis of rheumatic fever is based on modified “Jones Criteria” and requires either two major manifestations, or two minor and one major manifestations as well as the evidence of Type-A streptococcal infection (GAS). Diagnostic tests include: Testing for evidence of a GAS infection; ECG; echocardiography; ESR; and C-reactive protein.

“Jones criteria” major findings[41]: ● Carditis. ● Chorea. ● Erythema marginatum.

● Polyarthritis. ● Subcutaneous nodules.

“Jones criteria” minor findings: ● Polyarthralgia. ● Elevated ESR. ● Fever. ● Prolonged PR interval on ECG.

The protocol for treating acute rheumatic fever includes antibiotics, aspirin and corticosteroids.


endocarditisEndocarditis is the inflammation of the inner lining of the heart and the heart valves [42]. Endocarditis rarely occurs when the heart is healthy: Inflammation occurs when bacteria or fungi enter the bloodstream and

attach to abnormal heart valves or damaged heart tissue. There are two types of endocarditis: Infective and non-infective.

Infective endocarditis[42]

Two predisposing factors are necessary for infective endocarditis: An abnormality of the endocardium; and bacteria or fungi in the bloodstream. Risk factors include: Congenital abnormalities of the heart; rheumatic valvular disease; bicuspid aortic valves; cardiomyopathy; prior endocarditis; and artificial heart valves. Microorganisms which infect the heart usually originate from distant sites of infection such as gum disease or tooth decay, urinary tract infections, central venous lines, medical and surgical procedures, dental procedures, and intravenous drug usage. The most common organisms involved are streptococci bacteria, staphylococci bacteria, and various fungal infections.

Pathophysiology: The first step in the pathogenesis of endocarditis is damage or injury to the heart valves. This damage leads to local deposition of platelets and fibrin [42]. These sterile vegetations become infected by bacteria when pathogens enter the blood-stream. The organisms and vegetations become covered by a thin layer of fibrin and platelets (i.e. biofilm) which prevents an adequate immune response.

Local consequences of infective endocarditis: The consequences can be the formation of myocardial abscesses and the destruction

of cardiac tissue, leading to conduction abnormalities and valvular incompetence. These can in turn lead to heart failure and death.

Systemic consequences of infective endocarditis: The most serious systemic complication is the embolization of infected material to distant sites. On the right side of the heart, this results in pulmonary emboli leading to pulmonary infarction. On the left side of the heart, this results in systemic emboli to the spleen, kidney, and central nervous system. Retinal emboli are also common.

Endocarditis is classified according to its onset: ● Acute bacterial endocarditis: Starts suddenly and progresses

rapidly, and the source of infection is usually apparent. It can affect normal heart valves, although it is rare and occurs in only ten percent of cases.

● Subacute bacterial endocarditis: Develops and progresses slowly; often the source of infection entry is not apparent. This is the most common form of endocarditis and it accounts for 90% of cases.

● Prosthetic valvular endocarditis: Develops in a small percentage of patients following valve replacement.

Symptoms and clinical signs of infective endocarditisThe biggest variant in the different types of infective endocarditis is their onset. Initially, symptoms are non-specific such as a low-grade fever, night sweats, malaise, and weight loss with or without arthralgia and chills. The initial signs of endocarditis include fever, valvular incompetence or regurgitation, heart murmurs, and tachycardia. Retinal emboli can be seen upon funduscopy and are characterized by Roth spots which have small white centers. Skin manifestations include petechiae of the trunk, mucous membranes, and extremities.

Painful subcutaneous nodules at the tips of the fingers and toes are called Osler nodes, and non-tender macules on the palms of the hands and soles of the feet are called Janeway lesions and splinter hemorrhages when under the nails. Transient ischemic attacks of the CNS can occur. Emboli traveling to the kidneys can lead to flank pain and emboli to the spleen can result in upper quadrant pain. Long-term consequences of endocarditis include clubbing of the fingers and/or toes and splenomegaly.

Diagnosis, prognosis, and treatment of endocarditisThe symptoms and signs of endocarditis are non-specific so a variety of tests need to be performed to confirm the diagnosis. Blood cultures are used to confirm the presence of infection and these are done in combination with a complete blood count to confirm elevated white blood cells (i.e. infection) and anemia. A chest x-ray is done to determine evidence of cardiac enlargement and an ECG can detect irregular heart beat and tachycardia. An echocardiogram

is used to detect vegetation on the heart valves. All these diagnostic tests, combined with the clinical findings are needed to confirm the diagnosis of endocarditis [42].

Prognosis of infective endocarditis is usually poor even with correct diagnosis and treatment. Treatment involves prolonged (e.g. two to eight weeks) intravenous antibiotics specific to the organism involved. Valve debridement, repair and/or replacement may also be necessary.

myocarditisInflammation of the middle layer of the heart, i.e., the cardiac muscle, is known as myocarditis [43]. It can affect the heart muscle cells and the conduction system of the heart, causing heart failure and arrhythmias.

The causes of myocarditis are viral, bacterial and/or parasitic infection of the myocardium.

the causes of myocarditis[43]

The most common viral cause is infection with coxsackie B virus. Other viral causes include infection with parvovirus B19, epstein-barr virus, echoviruses and rubella virus. The human immunodeficiency virus (HIV) commonly causes myocarditis in patients who have progressed to utoimmune deficiency syndrome (AIDS). The most

common bacterial causes are staphylococcus spp. and streptococcus spp. infections. Parasitic causes include trypanosoma cruzi, and toxoplasma gondii and fungal causes include infection with candida and histoplasma spp.


the pathophysiology of myocarditisMyocarditis is caused by an autoimmune inflammatory response to a viral or bacterial infection [44]. During this inflammatory response, T-cells and cytokines target the myocardium; this can result in myocyte

death and damage to the myocardium. Undiagnosed myocarditis can lead to heart failure and death.

Symptoms and clinical signs of myocarditis Many cases of myocarditis are initially asymptotic, or there is evidence of a mild viral infection, e.g. a headache, general body pain, joint pain, fever, and sore throat [43]. Shortness of breast is usually the first symptom associated with myocarditis followed by chest pain, irregular

heart-beat, and swelling of the ankles and feet. Clinical signs of acute heart failure due to myocarditis include tachycardia and valvular regurgitation or heart murmurs [45].

tests used for the diagnosis of myocarditis[43]

● Blood tests: A complete blood count may show evidence of eosinophilia (rare) as well as an elevated erythrocyte sedimentation rate and elevated cardiac enzymes. In cases of viral infection, viral antibody titers will be detectable and/or elevated.

● ECG: An electrocardiogram may show tachycardia, ST segment elevation, and T wave changes, but these are generally non-specific.

● Echocardiogram: This is used to exclude other causes of heart failure and to evaluate cardiac function.

● Scintigraphy: This is used to diagnose inflammation of the myocardium. It is very accurate.

● Endomyocardial biopsy (EMB): Biopsy of the myocardium is the gold standard for the diagnosis of myocarditis.

treatment and complications of myocarditis[44]

Antibiotics, antimicrobials and antiviral medications are prescribed according to the type of infection diagnosed. Immunoglobulins and steroids are used to treat inflammation. Health care professionals

also provide supportive treatment for heart failure and arrhythmias. Myocarditis can result in permanent damage to heart muscle and result in heart failure, stroke, arrhythmias, and sudden death.

PericarditisThe outermost layer of the heart is known as the pericardium, and consists of two layers. The outer layer is fibrous and the inner layer is serous and the space between these two layers is the pericardial cavity which normally contains less than 50mL of pericardial fluid. The

pericardium supports and protects the heart. In pericarditis, there is inflammation of the pericardium, usually accompanied by an effusion in the pericardial cavity [46].

types of pericarditisAcute pericarditis can be fibrinous or effusive and the types of effusions are either serous, purulent, or hemorrhagic. Chronic

pericarditis is also known as constrictive pericarditis and is characterized by a thick fibrous pericardium.

Causes of pericarditis[46]

The most common causes of pericarditis include: Infection (e.g. bacterial, viral, or fungal); cancer; high dose radiation exposure to the chest; autoimmune disease (e.g. systemic lupus erythematosus,

rheumatoid arthritis, or rheumatic fever); certain drugs; myocardial infarction; and trauma to the chest (e.g. surgery). The causes of pericarditis are often unknown, i.e. idiopathic, or viral.

Pathogenesis of pericarditisThe pericardium is attacked by an infectious or unknown agent causing an inflammatory response and the release of the chemical mediators of inflammation. As the inflammation progresses, it leads vasodilation, hyperemia, edema, and the formation of an exudate.

Finally, the inflammation resolves but can be replaced by fibrous tissue and scarring. The most common complication of acute pericarditis is pericardial effusion

Symptoms and clinical signs of pericarditisAcute pericarditis is characterized by a sharp stabbing pain over the sternum with radiation to the neck, arms and back. It is different from the pain of myocardial ischemia in that it is sharp and stabbing, and made worse with deep inspiration. This is characteristic of pleuritic pain. Other symptoms include heart palpitations, fever, generalized malaise, cough, and peripheral edema [46]. The classic sign of pericarditis is a pericardial friction rub, which is audible upon auscultation of the heart. Pericardial friction rub is caused by the layers of the pericardium rubbing together. Other signs of pericarditis resemble those of heart failure.

Tests used for the diagnosis of pericarditis[46]

● ECG: The ECG may show elevated ST segments and diminished QRS segments corresponding to pericardial effusion.

● Chest x-ray: Enlargement of the heart is seen on CXR. ● Echocardiogram: An echocardiogram can be used to visualize

fluid in the pericardial cavity and can be used to diagnose an enlarged heart.

● CT scan: A CT scan is able to provide more detailed imaging of the heart and also used to exclude other abnormalities.

● Cardiac MRI: This can be used to diagnose thickening and inflammation of the pericardium.


Complications of pericarditis[46]

The complications of pericarditis are life-threatening, and early diagnosis is key to preventing complications. Constrictive pericarditis occurs with chronic scarring of the pericardium. The accumulation

of fluid in the pericardial cavity, i.e. pericardial effusion, leads to constriction of the heart and inadequate filling, causing a sudden drop in blood pressure, i.e. cardiac tamponade.

treatment of acute pericarditis[46]

Bedrest for the duration of the fever, and medication to decrease inflammation of the pericardium are common treatments for pericarditis. Anti-inflammatories are used to treat mild pericarditis. Colchicine can be used to reduce inflammation; this also reduces the risk of recurrence, but is not safe for use in those with kidney disease

or those taking certain medications. Corticosteroids are reserved for more severe cases of pericarditis. Treatment of cardiac tamponade is an emergency pericardiocentesis where the fluid is drained from the pericardial cavity and antibiotics are injected locally into the pericardial cavity.

Clinical manifestations of cardiac tamponadeBeck’s Triad consists of low blood pressure with narrowing pulse pressure, an increase in central venous pressure with distention of the neck veins, and muffled heart sounds. Other signs and symptoms include: Difficulty with breathing when supine, i.e. orthopnea; sweating, i.e. diaphoresis; anxiety; cyanosis; a rapid, weak peripheral

pulse rate; and a pulses paradox, i.e. blood pressure decreases with inspiration. The tests used to diagnose cardiac tamponade are the same as those used for the diagnosis of pericarditis. Characteristically there are ST elevation on ECG with no Q waves.

DISOrDerS OF CArDIAC StruCture

valvular heart diseases[47]

The flow of blood through the heart is regulated by four heart valves. On the right side of the heart are the tricuspid valve and pulmonary valve, and on the left side of the heart are the mitral and aortic valves. When these valves do not open correctly, it is known as stenosis and when these valves do not close correctly, it is known as regurgitation

or incompetence. Occasionally a valve can have both stenosis and regurgitation. Valves can be replaced by either mechanical valves or bio-prosthetic valves harvested from a pig or a cow. Mechanical valves require the use of anticoagulants.

Table 1. Descriptions of valvular heart diseases[47].

Etiology Symptoms Diagnosis Complications Treatment

Mitral regurgitation. Mitral valve prolapse; rheumatic fever; LV dilation.

Asymptomatic. Physical exam; murmur at apex; echocardiogram.

Heart failure; arrhythmias;

endocarditis.

Mitral valve replacement.

Mitral stenosis. Rheumatic fever. Heart failure. Physical exam; murmur at apex; echocardiogram.

Pulmonary hypertension; atrial fibrillation; thromboembolism.

Diuretics; aldosterone agonists;rarely requires valve replacement.

Tricuspid regurgitation. Dilation of the RV. Often asymptomatic. Physical exam; echocardiogram; holosystolic murmur.

Rare. Rarely requires valve replacement.

Tricuspid stenosis Rheumatic fever. Neck fluttering; fatigue; cold skin.

Physical exam; echocardiogram; presystolic murmur.

Rare. Diuretics; aldosterone agonists;rarely requires valve replacement.

Pulmonary regurgitation. Pulmonary hypertension. Asymptomatic. Physical exam; echocardiogram; decrescendo diastolic murmur.

Right-sided heart failure. Aortic valve replacement.

Pulmonary stenosis. Congenital. Asymptomatic until adult-hood. Crescendo-decrescendo murmur. Rare. Balloon valvuloplasty.

Aortic regurgitation. Valvular degeneration; rheumatic fever; endocarditis; marfan syndrome.

Dyspnea; orthopnea; paroxysmal nocturnal dyspnea; palpitations; chest pain.

Physical exam; echocardiogram; widened pulse pressure; early diastolic murmur.

Left ventricular hypertrophy;Left-sided cardiac failure.

Aortic valve replacement.

Aortic stenosis. Congenital; rheumatic fever. Syncope; angina; exertion dyspnea.

Physical exam; echocardiogram; crescendo decrescendo murmur.

Cardiac failure; arrhythmias. Balloon valvuloplasty; aortic valve replacement.

Cardiomyopathy[48]

Cardiomyopathy is a disorder of the heart muscle. There are three types of cardiomyopathy, dilated, hypertrophic, and restricted and these are based on pathology. The clinical symptoms and signs of

cardiomyopathy are the same as those found with heart failure, but they can present with chest pain, syncope, and sudden death.

Dilated cardiomyopathy[49]

This is also known as congestive cardiomyopathy and is caused by severe damage to the myocardial muscle cells of the ventricles. The ventricles enlarge or dilate and weaken (over time this includes the

atria), and are unable to pump sufficient blood, leading to heart failure. Dilated cardiomyopathy usually affects both ventricles.

Dilated cardiomyopathy etiology and pathophysiologyThe most common causes include coronary artery disease, viral infections, and hormonal disorders. Regardless of the cause, the myocardium dilates and hypertrophies in compensation for the loss of

function. Mural thrombi commonly form in the walls of the ventricles; this is further complicated by arrhythmias.


Dilated cardiomyopathy symptomsSymptoms depend on the side of the heart most affected and often present with atypical chest pain.

Dilated cardiomyopathy testsA chest x-ray shows cardiomegaly and the ECG may show sinus tachycardia and ST-segment depression. An echocardiogram shows

evidence of cardiac dilation and a cardiac MRI shows evidence of abnormal cardiac tissue.

Dilated cardiomyopathy prognosis and treatmentThe prognosis for DCM is poor a 20% death rate in the first year of diagnosis. Treat the underlying causes, treat heart failure and use anticoagulants if necessary.

Hypertrophic cardiomyopathy[50]

The features of hypertrophic cardiomyopathy include ventricular hypertrophy with diastolic dysfunction.

Hypertrophic cardiomyopathy etiology and pathophysiology The most common causes of hypertrophic cardiomyopathy are congenital abnormalities. The most marked characteristic is hypertrophy of the upper ventricular septum; this results in a stiff

ventricle with decreased filling, causing an increase in pulmonary venous pressure. Cardiac output decreases over time.

Hypertrophic cardiomyopathy symptomsThe usual age of presentation is during infancy and adolescence, and the classic symptoms include chest pain, shortness of breath (i.e. dyspnea), palpitations, syncope, and even sudden death.

Hypertrophic cardiomyopathy diagnostic tests and treatmentCardiac MRI is the diagnostic test of choice as it is able to detect damaged myocardium. The aim of treatment is to decrease cardiac contractility and allow for increased filling of the ventricles. Diuretics,

ACE-inhibitors, and Angiotensin II blockers should be completely avoided because they decrease left ventricular size and function.

restrictive cardiomyopathy[51]

Restrictive cardiomyopathy is characterized by stiff and/or non-compliant ventricular walls, causing a decrease in ventricular filling, especially on the left. The cause is usually unknown.

restrictive cardiomyopathy pathophysiologyThere is decreased ventricular filling from a thick or hypertrophied ventricle. Endocardial thickening can also occur, leading to mitral and

aortic valve regurgitation. Mural thrombi can form as well, causing systemic emboli.

restrictive cardiomyopathy symptomsThe most common presenting symptom is exertion fatigue.

restrictive cardiomyopathy diagnostic tests and treatment Diagnosis is made by an echocardiogram. Without identifying the cause, treatment is often unsuccessful, but diuretics can be used, with caution, to avoid lowering preload.

Arrhythmias[52]

The term arrhythmia refers to any change in the normal electrical activity of the heart. Any abnormal electrical activity directly affects

cardiac function by causing a decrease in the blood pumped to the rest of the body. This can cause organ damage due to under-perfusion.

types of arrhythmias ● Atrial fibrillation: The atria contract irregularly. ● Bradycardia: Heart rate is <60 beats/min. ● Tachycardia: Heart rate is >100 beats/min.

● Ventricular fibrillation: The ventricles contract irregularly. ● Premature contraction: The heart contracts early.


etiology of arrhythmias [52]

Any heart disorder, e.g. congenital or acquired, can affect rhythm. Systemic conditions that affect rhythm include: Electrolyte abnormalities (e.g. low potassium, low magnesium); hypoxia;

hormonal disturbances (e.g. thyroid); and drugs or substances including alcohol and caffeine [53].

Pathophysiology of arrhythmias[54]

Normally, electrical conduction begins at the sinoatrial node (the “heart’s natural pacemaker”). In certain conditions the sinoatrial node develops an abnormal rhythm or other cells in the myocardium begin

their own electrical activity, so that another portion of the heart acts as a pacemaker. Rhythm abnormalities are caused by abnormalities of impulse formation, impulse conduction, or a combination of both.

Symptoms of arrhythmiasRhythm disorders are often asymptomatic, but can cause palpitations, shortness of breath, syncope, and cardiac arrest.

Diagnostic tests and treatment of arrhythmiasThe clinical diagnosis of arrhythmia is usually made by ECG. The basis for treating any arrhythmia is to normalize electrolytes, control atrial and ventricular contraction, and give appropriate medication[57]. Sinus tachycardia occurs as a compensatory response to heart

failure and if it does not subside with treatment for heart failure, the underlying cause needs to be investigated. Generally, it is then treated with beta blockers.

Atrial fibrillationAtrial fibrillation is the most common cause of arrhythmia and can have serious consequences such as stroke, heart failure, and other heart

complications [54,55]. It is characterized by an irregular, rapid heart rate caused by the two atria contracting out of sync with the ventricles.

Atrial fibrillation etiologyAbnormalities and damage to the heart structure are the most common causes of atrial fibrillation, but in some cases the cause is unknown.

Symptoms of atrial fibrillationMany people with atrial fibrillation have no symptoms; however, the most common symptoms are palpitations, weakness, reduced exercise tolerance, dizziness, and chest pain.

Atrial fibrillation pathophysiologyIn atrial fibrillation, the atria receive abnormal electrical contraction signals, causing the atria to quiver. As a result, the atrioventricular node (i.e. the node that conducts the signal between the atria and the ventricles) also receives abnormal electrical contraction signals. The result is a rapid and irregular heart rate, usually between 100-175

beats per minute. Atrial flutter is similar to atrial fibrillation, but the electrical signals are less irregular. The risk factors for atrial fibrillation are the same as those for any heart disorder, but there are hereditary elements.

Atrial fibrillation complicationsThe most serious consequence of atrial fibrillation is stroke followed by heart failure.

Atrial fibrillation diagnostic testsAn ECG is the gold standard for the diagnosis of atrial fibrillation; however, because atrial fibrillation can be erratic, it is often diagnosed

by a halter-monitor which is a wearable 24-hour ECG monitor. In terms of blood tests, it is important to rule out thyroid disorders.

Atrial fibrillation treatment The goal for treatment of atrial fibrillation is to reset the normal heart rhythm and prevent blood clots. Heart rhythm can be reset using electrical cardioversion. This is an event where the heart is shocked back into normal rhythm while the patient is under sedation.

Rhythm can also be reset with pharmacologic cardioversion using anti-arrhythmic drugs. Anticoagulants are used to prevent blood clot formation.

Ventricular fibrillation[56]

Ventricular fibrillation is a cardiac electrical conduction disorder where the heart beats non-uniformly and/or erratically. As a result of the irregular beats, the ventricles quiver and are unable to pump blood

to the rest of the body. Ventricular fibrillation is a life-threatening emergency.


Ventricular fibrillation etiologyIn most cases of ventricular arrhythmia, the underlying cause is damage to the heart from a previous myocardial infarction which caused scarring of the heart muscle tissue.

Ventricular fibrillation risk factorsRisk factors for ventricular fibrillation include previous heart attack, previous episode of ventricular fibrillation, cardiomyopathy, illegal drug use, and/or electrolyte abnormalities.

Pathophysiology of ventricular fibrillationUnderlying damage to the myocardium can lead to distortion of the electrical impulses from the AV node, causing irregular or erratic

electrical activity where the ventricles contract out of rhythm with the atria.

Ventricular fibrillation symptomsSymptoms of ventricular fibrillation include chest pain, tachycardia, dizziness, nausea, shortness of breath, and loss of consciousness.

Ventricular fibrillation diagnosisVentricular fibrillation must be diagnosed in an emergency situation [56]. An ECG is used to diagnose ventricular fibrillation, but this usually happens after cardiopulmonary resuscitation and defibrillation.

Other cardiac tests, including echocardiogram, cardiac catheterization, blood tests and cardiac MRI are conducted after the patient is stabilized.

Treatment of ventricular fibrillation after emergency stabilizationAnti-arrhythmic drugs as well as beta-blockers are used to stabilize the patient. An implantable cardioverter monitors heart rhythm, and if the heart rate is too low, it sends out low grade electrical shocks to correct

the heart’s pace. Coronary angiography and stent placements are used when there is underlying coronary artery disease and coronary artery bypass surgery is performed if necessary.

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32. Statins: Are These Cholesterol-lowering Drugs Right for You? Mayo Clinic. Web. 23 May 2016: http://www.mayoclinic.org/statins/art-20045772.

33. Statin Side Effects: Weigh the Benefits and Risks. Mayo Clinic. Web. 23 May 2016: http://www.mayoclinic.org/statin-side-effects/art-20046013.

34. Deep Venous Thrombosis. University of Maryland Medical Center. Web. 24 May 2016: http://umm.edu/health/medical/ency/articles/deep-venous-thrombosis.

35. Deep Venous Thrombosis (DVT). Merck Manuals Professional Edition. Web. 23 May 2016: http://www.merckmanuals.com/professional/cardiovascular-disorders/peripheral-venous-disorders/deep-venous-thrombosis-dvt.

36. Stroke. Symptoms and Causes. 2016. Web. 23 May 2016: http://www.mayoclinic.org/diseases-conditions/stroke/symptoms-causes/dxc-20117265.

37. Pulmonary Embolus. University of Maryland Medical Center. Web. 24 May 2016: http://umm.edu/health/medical/ency/articles/pulmonary-embolus.

38. Rheumatic Fever. Mayo Clinic. Web. 24 May 2016: http://www.mayoclinic.org/diseases-conditions/rheumatic-fever/basics/definition/con-20031399.

39. Rheumatic Fever. Risk Factors. Web. 24 May 2016: http://www.mayoclinic.org/diseases-conditions/rheumatic-fever/basics/risk-factors/con-20031399.

40. Pathology of Rheumatic Heart Disease. Overview, Etiology and Pathophysiology, Clinical Features. Web. 24 May 2016: http://emedicine.medscape.com/article/1962779-overview.

41. Rheumatic Fever. Merck Manuals Professional Edition. Web. 24 May 2016: http://www.merckmanuals.com/professional/pediatrics/miscellaneous-bacterial-infections-in-infants-and-children/rheumatic-fever.

42. Infective Endocarditis. Merck Manuals Professional Edition. Web. 25 May 2016: https://www.merckmanuals.com/professional/cardiovascular-disorders/endocarditis/infective-endocarditis.

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Appendix 1: Protocol for the management of Hypertension: http://millionhearts.hhs.gov/files/

Hypertension-Protocol.pdf.


1. The primary event leading to atherosclerosisa. Recent pregnancy.b. Coronary artery disease.c. Hypertension.d. Repeated damage to the artery wall.

2. Which of the lipids are cardio-protective?a. LDL.b. HDL.c. Cholesterol.d. Triglycerides.

3. Hypertension is defined as?a. Cardiac output x stroke volume.b. Stroke volume x total peripheral resistance.c. After load – preload.d. Cardiac output x total peripheral resistance.

4. What is the most common type of hypertension?a. Primary hypertension.b. Secondary hypertension.

5. What is the first line test for diagnosing myocardial ischemia?a. Exercise stress test.b. Echocardiogram.c. ECG.d. Ultrasound.

6. What is he most common symptom of peripheral artery disease?a. Vague leg pain.b. Claudication.c. Pins and needles.d. Numbness.

7. What is the most common predisposing factor for deep venous thrombosis?a. Inadequate nutrition.b. Inadequate rest after exercising.c. Immobility.d. Sedentary lifestyle.

8. What is the most common complication of acute pericarditis?a. Hepatomegaly.b. Renal failure.c. Pericardial effusion.d. Cardiomegaly.

9. What is the most common heart valve affected in rheumatic fever?a. Aortic valve.b. Mitral valve.c. Tricuspid valve.d. Pulmonary valve.

10. What are one of the major Jones criteria for rheumatic fever?a. Elevated ESR.b. Carditis.c. Fever.d. Polyarthralgia.

PAtHOPHySIOLOgy OF tHe CArDIOvASCuLAr SyStemFinal examination Questions

Select the best answer for questions 1 through 10 and mark you answers online at nursing.elitecme.com.

ANCCFL04CSE17


NOTES

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Chapter 6: Pathophysiology of the Cardiovascular System · 2016-12-20 · Page 115 nursing.elitecme.com Chapter 6: Pathophysiology of the Cardiovascular System 4 Contact Hours Release