COMAT Internal Medicine

COMAT Internal Medicine

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TABLE OF CONTENTS Preface........................................................................................................ 1 Preparing for the Examination.................................................................... 4 Chapter One: Cardiovascular Conditions .................................................... 5 Acute Coronary Syndromes ............................................................................................. 5 Arrhythmias ..................................................................................................................... 7 Angina Pectoris .............................................................................................................. 15 Hyperlipidemia .............................................................................................................. 16 Peripheral Vascular Disease .......................................................................................... 18 Congestive Heart Failure ............................................................................................... 19 Aortic Dissection ............................................................................................................ 22 Valvular Heart Disease .................................................................................................. 23 Pericarditis ..................................................................................................................... 24 Endocarditis ................................................................................................................... 26 Key Takeaways ............................................................................................................... 29 Quiz ................................................................................................................................ 30 Chapter Two: Endocrine Conditions ......................................................... 33 Weight Gain or Loss ....................................................................................................... 33 Adrenal Disorders .......................................................................................................... 36 Diabetes Mellitus ........................................................................................................... 40 Parathyroid Diseases ..................................................................................................... 43 Thyroid Diseases ............................................................................................................ 46 Pituitary Disorders ......................................................................................................... 49

Male Gonadal Disorders ................................................................................................ 51 Female Gonadal Disorders ............................................................................................ 52 Quiz ................................................................................................................................ 55 Chapter Three: Gastrointestinal Conditions .............................................. 58 Diseases of the Esophagus ............................................................................................. 58 Diseases of the Stomach ................................................................................................ 61 Malabsorption ................................................................................................................ 62 Constipation and Diarrhea ............................................................................................ 66 Inflammatory Bowel Disease ......................................................................................... 69 Liver Diseases ................................................................................................................ 73 Pancreatic Diseases ........................................................................................................ 76 Gallbladder Disorders .................................................................................................... 78 Gastrointestinal Cancer ................................................................................................. 81 Key Takeaways ............................................................................................................... 84 Quiz ................................................................................................................................ 85 Chapter Four: Hematology/Oncology Conditions ...................................... 88 Coagulation Disorders ...................................................................................................88 Anemia ........................................................................................................................... 92 Basics of Cancer from a Molecular Level....................................................................... 97 Blood-related Malignancies ......................................................................................... 100 Lymphomas...................................................................................................................101 Leukemia ...................................................................................................................... 103 Cancer Screening Recommendations .......................................................................... 107 Key Takeaways ............................................................................................................. 109

Quiz ...............................................................................................................................110 Chapter Five: Infectious diseases Conditions ........................................... 113 Common Viral Infections.............................................................................................. 113 Common Bacterial Infections ....................................................................................... 117 Tuberculosis .................................................................................................................. 121 Common Fungal Infections ......................................................................................... 123 Parasitic Infections ...................................................................................................... 124 HIV Disease.................................................................................................................. 125 Bioterrorism ..................................................................................................................127 Infectious Disease Prevention Strategies .....................................................................127 Key Takeaways ............................................................................................................. 130 Quiz ............................................................................................................................... 131 Chapter Six: Musculoskeletal Conditions ................................................ 134 Osteoporosis................................................................................................................. 134 Somatic Dysfunction .....................................................................................................137 Viscerosomatic Reflexes .............................................................................................. 139 Inflammatory Rheumatic Diseases ............................................................................. 140 Rheumatoid Arthritis ................................................................................................... 140 Gout and Pseudogout ................................................................................................... 142 Non-inflammatory Rheumatic Diseases ..................................................................... 145 Vasculitis ...................................................................................................................... 147 Giant Cell Arteritis ....................................................................................................... 149 Fibromyalgia ................................................................................................................ 150 Autoimmune Myositis .................................................................................................. 151

Endocrine-mediated Myopathy ................................................................................... 152 Key Takeaways ............................................................................................................. 154 Quiz ...............................................................................................................................155 Chapter Seven: Neurological Conditions ................................................. 158 Stroke ........................................................................................................................... 158 Intracerebral Hemorrhage ............................................................................................ 161 Spinal Cord Diseases.................................................................................................... 163 Peripheral Nerve Diseases ........................................................................................... 165 Neuromuscular Junction Disorders ............................................................................ 168 Guillain-Barre Disease ................................................................................................. 169 Small Fiber Sensory Neuropathy ................................................................................. 170 Disorders of Cerebral Function .................................................................................... 171 Delirium ........................................................................................................................173 Dysautonomias .............................................................................................................175 Key Takeaways .............................................................................................................. 181 Quiz .............................................................................................................................. 182 Chapter Eight: Renal Diseases and Hypertension .................................... 185 Fluid and Electrolyte Disorders ................................................................................... 185 Acute Kidney Injury ..................................................................................................... 189 Chronic Kidney Disease ................................................................................................ 191 Renal Calculi ................................................................................................................ 193 Glomerular and Tubulointerstitial Diseases ............................................................... 195 Obstructive Uropathy .................................................................................................. 197 Arterial Hypertension .................................................................................................. 199

Key Takeaways .............................................................................................................202 Quiz .............................................................................................................................. 203 Chapter Nine: Respiratory Diseases ........................................................ 206 Asthma .........................................................................................................................206 COPD ............................................................................................................................ 210 Interstitial Lung Disease .............................................................................................. 213 Pneumonia ................................................................................................................... 216 Pulmonary Embolism .................................................................................................. 218 Respiratory Failure ......................................................................................................220 Respiratory Tract Cancer ............................................................................................. 221 Key Takeaways ............................................................................................................. 224 Quiz .............................................................................................................................. 225 Chapter Ten: Allergy and Skin Conditions ............................................... 228 Atopic Diseases ............................................................................................................ 228 Anaphylaxis .................................................................................................................. 231 Drug and Food Allergies .............................................................................................. 234 Benign Skin Rashes ...................................................................................................... 236 Common Benign Skin Lesions ..................................................................................... 241 Skin Cancers ................................................................................................................. 247 Key Takeaways ............................................................................................................. 252 Quiz .............................................................................................................................. 253 Summary ................................................................................................ 256 Course Quiz ............................................................................................ 259 Answers to Quiz ...................................................................................... 310

Chapter One ................................................................................................................. 310 Chapter Two ................................................................................................................. 312 Chapter Three .............................................................................................................. 314 Chapter Four ................................................................................................................ 315 Chapter Five ................................................................................................................. 316 Chapter Six ....................................................................................................................317 Chapter Seven .............................................................................................................. 319 Chapter Eight ............................................................................................................... 320 Chapter Nine ................................................................................................................ 322 Chapter Ten .................................................................................................................. 324 Course Quiz .................................................................................................................. 325

PREFACE The purpose of this course is to prepare the osteopathic student studying for the COMAT Internal Medicine Examination. Internal medicine is the study of common and uncommon adult diseases of the major organ systems of the body. The osteopathic student has the dual obligation to understand these disorders from an osteopathic and allopathic perspective so the course addresses these dualities as part of what you’ll need to learn and understand.

The different organ systems in this course include the cardiovascular system, the respiratory system, the gastrointestinal system, the nervous system, the musculoskeletal system, and the endocrine system, among others. We will talk about the major diseases of these body areas that you will encounter as part of a typical osteopathic practice.

These are things you probably have encountered to some degree as part of your classroom education and student clinical experiences. The course itself is designed to put these two things together in a meaningful way so you can pass the exam with confidence, based on the commonly accepted ways to manage these health conditions in a clinical setting.

The focus of chapter one in the course is the different cardiovascular diseases you will encounter in a typical internal medicine practice. It includes conditions like angina, acute coronary syndromes, and arrhythmias as well as congestive heart failure, aortic dissection, valvular heart disease, and peripheral vascular disease. Inflammatory conditions affecting the heart, such as endocarditis and pericarditis, are less common but may still be seen and managed by you in an internal medicine practice. These are also covered in this chapter.

Chapter two involves a discussion of the different endocrine disorders you might encounter in an internal medicine setting. These include disorders of weight loss or weight gain, diabetes mellitus, diseases of the parathyroid glands, thyroid disorders, endocrine diseases of pituitary origin, adrenal gland disorders, and the different male and female gonadal diseases related to the endocrine system. As you will see in this

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chapter, the symptoms can overlap or can be vague, requiring astute observation and laboratory measurements in order make a diagnosis and treat the different diseases.

Chapter three in the course introduces the different gastrointestinal diseases you would encounter in a general internal medicine setting. Things we talk about in this chapter include esophageal and stomach disorders, malabsorption, common bowel disorders like constipation and diarrhea, and inflammatory bowel disease. Diseases unrelated to the alimentary canal itself are also covered, including liver disease, pancreatic diseases, and gallbladder disorders. Common GI cancers are also covered in this chapter.

The focuses of chapter four are hematological conditions and oncological disorders.

Hematological disorders discussed in the chapter include anemias, coagulation disorders, and blood-related malignancies. The general management of cancer including the recommended cancer screening tests in the US are also covered as part of this chapter.

Chapter five in the course talks about the different infectious diseases a person can have, including viral infections, bacterial infections, fungal infections, and parasitic infections.

Certain types of infectious disease situations are discussed specifically, such as HIV disease. Issues related to bioterrorism and infectious disease prevention are also covered in this chapter.

Chapter six involves a thorough discussion of musculoskeletal conditions as they are approached in both internal medicine and osteopathy. These include coverage of somatic dysfunctions and viscerosomatic relationships in musculoskeletal diseases.

Other common disorders covered in this chapter include osteoporosis, rheumatic diseases, vasculitis, and several of the more common muscle disorders in human disease states.

The focus of chapter seven in the course is the different neurological conditions you might expect to see an internal medicine practice. Common disorders discussed in the chapter include the different types of stroke, the different types of dementia, and delirium. Less commonly seen disorders are those that affect the spinal cord, peripheral nerves, and the autonomic nervous system. You should be able to recognize and treat

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these disorders; this is why they are covered thoroughly in the chapter from discussing presentation to diagnostic testing to treatment of these challenging disorders.

Chapter eight in the course focuses on kidney diseases and hypertension. Kidney diseases can cause electrolyte disturbances or can simply be how the body responds to electrolyte disturbances caused by other dysfunctions in the body. Diseases discussed in this chapter include acute kidney injury, chronic kidney disease, kidney stones, obstructive uropathy, and intrinsic kidney diseases. While hypertension is not always related to the kidneys, much of the treatment of hypertension focuses on the kidneys, so this is covered in this chapter.

Chapter nine talks about the different respiratory diseases seen in internal medicine.

Some of the diseases talked about are acute diseases like asthma, pneumonia, respiratory failure, or pulmonary embolisms. Others are chronic diseases managed in internal medicine, such as COPD and interstitial lung disease. Also covered in the chapter are some of the major respiratory tract cancers, including the two main types of lung cancer.

Chapter ten in the course talks about the different allergy and skin-related diseases seen in clinical practice. Allergic diseases can involve systemic or respiratory symptoms as well as skin-related symptoms due to exposure to environmental allergens. There are several skin diseases discussed in this chapter, including skin rashes, benign skin lesions, and skin cancers, which have increased in incidence in recent years.

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PREPARING FOR THE EXAMINATION The COMAT internal medicine examination is designed to be taken after you have taken the prerequisite classroom education and after you have participated in a clinical rotation or clerkship in the field of internal medicine at your own college of osteopathic medicine or COM. The COMAT examination you take has been created by your COM and is designed to assess both your knowledge and skills in this area of medicine as well as how well your COM has presented the material to you as part of your education. The information you’ve learned and will demonstrate in the exam will be necessary to assimilate prior to entering an osteopathic or allopathic residency program after graduation.

There are two dimensions covered in the examination. The first of these is patient presentation and the second is called physician tasks. The areas involved in the patient presentation aspect of the exam are divided equally among the different body systems, while the physician task breakdown is divided into health promotion or disease prevention, history, physical exam, and diagnostics, management, and pathophysiology.

The majority of questions are based on diagnostic skills and management so these will be emphasized in this course.

The examination itself will consist of just 125 questions you will be asked to complete in 2.5 hours after a five-minute tutorial. The questions will be different from one COMAT examination to another and will differ in their level of difficulty but are designed to be reliable from test to test, regardless of which one you take.

The score you receive will be based on a mean score of 100 and a standard deviation of 10. Each test is validated and reviewed annually so as to be consistent over time and among the different examinations. On the NBOME website, there is a table that converts the mean score to a percentile rank. Using this table, you will see that a score of 100 is equivalent to being at the 50th percentile among other students. There is no real pass or fail aspect to this examination.

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CHAPTER ONE: CARDIOVASCULAR CONDITIONS The focus of this chapter is the different cardiovascular diseases you will encounter in a typical internal medicine practice. It includes conditions like angina, acute coronary syndromes, and arrhythmias as well as congestive heart failure, aortic dissection, valvular heart disease, and peripheral vascular disease. Inflammatory conditions affecting the heart, such as endocarditis and pericarditis, are less common but may still be seen and managed by you in an internal medicine practice. These are also covered in this chapter.

ACUTE CORONARY SYNDROMES Acute coronary syndromes are largely conditions you’ll manage in the emergency department or hospital, although it is possible you might see a person in an outpatient setting. When you see this in this setting, however, you need to recognize these as being emergency conditions requiring care in an acute care setting.

There are three separate conditions that can be called a type of acute coronary syndrome. These are unstable angina, non-ST-segment elevation MI or NSTEMI, and ST-segment myocardial infarction. Some will also include sudden cardiac death as being one of the acute coronary syndromes, even though the treatment strategy is different.

Unstable angina represents chest pain and related symptoms that do not involve true necrosis of muscle tissue. For this reason, there will be no increase in cardiac biomarkers and no evidence of infarction. The major definitions for this include resting angina greater than 20 minutes in total length, new-onset class 3 angina, or increasing angina that was once stable. Any type of ECG change may be seen but the issue is usually transient in nature. The biggest risk is in the transition between this and a completed myocardial infarction.

In a NSTEMI, the patient has, by definition, a subendocardial myocardial infarction.

There will be no ST segment elevation but the cardiac markers will be elevated. In a STEMI, the necrosis by definition will be transmural and the ECT finding will be that of 5

ST segment elevation. There will also be an elevation of cardiac markers. Figure 1 shows the difference between a STEMI and NSTEMI:

Figure 1.

Nearly all cases of acute coronary syndromes are due to atherosclerosis of one of the coronary arteries, usually because of a rupture of an unstable atherosclerotic plaque that leads to acute blockage. The severity of preexisting stenosis does not always predict such an event. Less common causes of the same problem are coronary artery embolism, coronary artery spasm, and dissection of a coronary artery. Coronary spasm is often due to cocaine abuse.

The symptoms you will see vary with the patient, the location of the infarct, and the size of the infarct. Common symptoms include chest pain or pressure, the urge to burp, a sense of indigestion, nausea, and radiation of the pain or pressure to the neck, jaw, left shoulder, or arms. There are many possible complications, including arrhythmias or conduction defects, myocardial dysfunction, which can happen for many reasons, and valvular disease, which usually involves mitral valve regurgitation from papillary muscle rupture.

Your diagnostic process starts with an ECG, which is usually serial. The cardiac markers should be assessed every 4 to 6 hours and, if there is evidence of a STEMI or complication like persistent pain, arrhythmia, or hypotension, the person should be sent for immediate angiography and possible percutaneous coronary intervention or PCI.

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The patient with unstable angina or a NSTEMI can have a delayed angiogram within 48 hours of admission.

While the ECG is most important, serial cardiac markers are also important. The main cardiac enzyme involved is the CK-MB enzyme, while markers of cell contents of myocardial cells include troponin I, myoglobin, and troponin T. These are seen at different times but the troponins are far more sensitive and are seen earlier in the bloodstream compared to the cardiac enzymes. In some case, the test is too sensitive and the chance of false positivity does exist. For this reason, the results seen must be balanced with the symptoms, risk factors, and ECG findings.

The coronary angiography is both diagnostic and therapeutic if combined with percutaneous coronary intervention. If done soon after an MI, it can effectively abort the process so that the amount of coronary damage will be minimized. Besides being able to resolve the ischemia, the angiography can assess the other coronary arteries as well as things like ejection fraction. Other imaging techniques, like echocardiography or radionuclide scanning, will not generally be helpful.

The treatment starts in the prehospital setting with aspirin, oxygen, nitrates and possible ECG to expedite diagnosis and further management. An IV is started and continuous cardiac monitoring is accomplished. Morphine was once suggested but there are adverse outcomes associated with it. Drug therapy can involve antiplatelet drugs like aspirin or clopidogrel, anticoagulant drugs, or fibrinolytics, such as tissue plasminogen activator. Many patients will have percutaneous coronary angiography, while a few will not be candidates for this and will require a coronary artery bypass graft or CABG.

ARRHYTHMIAS Cardiac arrhythmias can happen for a variety of reasons, including ischemic heart disease, congenital diseases of the heart, electrolyte abnormalities, toxins or drugs, and hormonal imbalances, such as low thyroid conditions and hyperthyroidism. Among drugs or toxins, both caffeine and alcohol are contributors to cardiac arrhythmias.

Cardiac tissues can be called fast-channel or slow-channel tissues. The fast-channel tissues are the working myocytes and the cells of the His-Purkinje system, which are 7

poor pacemakers but fast conductors of electricity. The slow-channel tissues are those of the SA or AV node, which are the traditional pacemaker cells that do not conduct electricity very well themselves. The SA node has the fastest rate of spontaneous depolarization so it will set itself up to be the pacemaker of the heart.

You should be familiar with the different types of arrhythmia you may encounter when evaluating the patient. Arrhythmias can be divided in different ways. For example, there are tachyarrhythmias, bradyarrhythmias, and rhythm disturbances that have no abnormalities in the overall rate. There are also wide-complex arrhythmias and narrowcomplex arrhythmias. Those that are more narrow-complex in appearance tend to originate prior to the AV node and tend to be faster, while wide-complex arrhythmias are secondary to an initiated rhythm below the AV node. These can be slow or fast.

Ventricular fibrillation and asystole are agonal rhythms that usually end in death unless a rhythm can be reestablished through defibrillation.

An atrioventricular nodal reentry tachycardia usually involves a premature P wave originating from somewhere in the atrium that gets propagated down the normal pathways but also cycles back to reenter the AV node much faster than a normal SA nodal impulse. This is generally a tachyarrhythmia made worse by sympathetic stimulation of the heart that shortens the refractoriness of the tissue.

The main symptom seen is palpitations, although if the rate is too fast, there will be chest discomfort, dyspnea, syncope, or presyncope. If prolonged, the patient will have a release of atrial natriuretic peptide and polyuria. You may see cannon waves, which are large jugular venous pulsations.

In any tachyarrhythmia, if the QRS is narrow, the origin of the disturbance is above the bifurcation of the His bundle branch. If the QRS is wide, the origin of the disturbance is ventricular. An alternative might be a supraventricular origin with some type of intraventricular conduction defect or a situation where there is ventricular preexcitation, such as is seen in Wolff-Parkinson-White or WPW syndrome. Figure 3 shows a typical ECG tracing in WPW syndrome:

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Figure 3.

Bradyarrhythmias happen when the heart rate is less than 60 beats per minute. We will talk further about the different types of heart block that can cause this. If there is no relationship between the P wave and QRS complex, this is a complete heart block. It leads to some type of escape rhythm. If the AV node is normal, the escape rhythm will be seen as a narrow QRS complex. If the escape rhythm is junctional and the AV node is not normal, the QRS will be wide. The QRS will be wide as well if the escape rhythm comes from below the AV node and is ventricular.

There are essentially four types of tachyarrhythmia that depend on four different issues.

These include regular rhythms versus irregular rhythms as well as narrow versus wide QRS complexes. Irregular, narrow QRS arrhythmias with a fast rhythm include the following: •

Atrial fibrillation involves a narrow complex tachyarrhythmia in the absence of any discrete P waves.

•

Atrial flutter involves the presence of sawtooth uniform P waves with variable conduction of these P waves but with a rate that is also usually too fast.

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•

Atrial tachycardia involves regular but abnormal P waves and variable conduction so that the QRS complexes will not be regular and the rate is usually less than 250 beats per minute.

•

Multifocal atrial tachycardia involves discrete P waves that come from different places in the atria so the P waves themselves will be different from beat to beat.

If the QRS complex is wide and the rhythm is irregular, it could mean that there is a bundle branch block or a situation of ventricular preexcitation. The more common thing seen, however, is polymorphic ventricular tachycardia.

When it comes to regular rhythms and narrow QRS complexes seen in tachyarrhythmias, you have four choices to consider, including the following: •

Sinus tachycardia, which involves P waves and normal QRS complexes but a rate that is greater than 100 beats per minute.

•

Atrial tachycardia is similar but the rate is faster and the AV conduction is consistent from beat to beat.

•

Atrial flutter can be present but, if the AV conduction ratio is the same from beat to beat, the rhythm will be regular.

•

In SVT or supraventricular tachycardia, there is a circular pathway that continually stimulates the AV node so the rate is rapid and regular. Figure 4 shows what paroxysmal SVT looks like:

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Figure 4.

Any of these tachyarrhythmias will have a regular rhythm but a wide QRS complex if there is a bundle branch block. In addition, if there is monomorphic ventricular tachycardia, as is seen in figure 5, the QRS complex will be wide but the rate will be regular:

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Figure 5.

Atrial fibrillation is worth looking at further because it is so common and because it is something you will help patients deal with on a chronic basis. Some patients will have no symptoms, while others will have weakness, palpitations, exercise intolerance, presyncope, and dyspnea at rest. The acute rhythm disturbance is far less dangerous to the patient than the long-term complication of thromboembolism, often leading to a high risk of stroke unless this risk is reduced.

In atrial fibrillation, the atria do not contract at all but, in most cases, the QRS complex will still be narrow. The rate is generally irregular and may or may not be fast. Atrial fibrillation affects more than 2 million people in the United States with an increasing prevalence with advancing age. The major complication is the formation of a thrombus inside the atria, which causes a risk of stroke that is about 7 percent per year. There is also the possibility of systemic emboli, such as those affecting the GI tract, kidneys, heart, and eyes. Cardiac output will decrease by 10 percent just because the atria do not contract. If the rate is too fast in addition, the cardiac output will further diminish.

In considering the etiology of atrial fibrillation, you need to consider that it can be caused by coronary artery disease, hypertension, cardiomyopathy, valvular disorders involving the mitral or tricuspid valve, binge drinking, or hyperthyroidism. There are rare causes of atrial fibrillation, including pericarditis, myocarditis, COPD, and pulmonary embolism. Atrial fibrillation can start with atrial flutter that degenerates to involve a fibrillating atrium.

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Atrial fibrillation can come in different forms. In paroxysmal atrial fibrillation, the duration is less than a week and the person spontaneously converts to sinus rhythm. In persistent atrial fibrillation, the duration is greater than a week and it does not convert itself. In long-lasting persistent atrial fibrillation, the duration is a year or more but restoration of normal rhythm can still occur. In permanent atrial fibrillation, restoration of normal rhythm is not possible.

In diagnosing atrial fibrillation, an ECG will detect the rhythm, while an echocardiogram can best show the presence of a thrombus in the atrial cavity. Thyroid function studies should also be done. The ECG will show a complete absence of P waves, usually associated with a narrow complex QRS pattern that is generally irregular.

Your treatment will be different, depending on what you want to achieve. In some cases, the goal is rate control only, which will control symptoms and reduce the risk of cardiomyopathy and hemodynamic instability. AV node blockers like any of the beta blockers or calcium channel blockers can be used. Digoxin is less effective but will help heart failure. Amiodarone will also be necessary as an anti-arrhythmic drug.

Another option is rhythm control, which involves synchronized cardioversion or antiarrhythmic drugs. Prior to doing this, you’ll need to prevent thromboembolism because cardioversion is associated with an increased risk of throwing off an embolism at the time of cardioversion. Anticoagulation should happen for 3 weeks before and 4 weeks after cardioversion. Class Ia and class III antiarrhythmic drugs can also be used instead of cardioversion but these are only effective about half the time.

Ablation procedures also work for atrial fibrillation. In such cases, the AV node can be ablated in order to precipitate complete heart block. In such cases, you must put in a pacemaker unless you ablate just one AV nodal pathway. There are advanced techniques that can be done, such as pulmonary vein isolation.

Long-term prevention of thromboembolism can involve warfarin or Coumadin therapy, which works well but requires frequent coagulation studies to be tested of the blood.

Other choices include apixaban, edoxaban, or rivaroxaban, which are also oral anticoagulants that do not require blood testing to be effective. Some patients can have a filter placed that will prevent passage of any clot beyond the filter.

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Atrioventricular block or AV block involves some type of separation between the atrial impulse and the ventricular impulse. Most commonly, this is caused by fibrosis of the conduction system of the heart but can be caused by ischemic heart disease. Other, less common causes, are drugs like beta blockers or calcium channel blockers, increased vagal tone, congenital heart disease, and valvular heart disease.

There are four different types of AV block, most of which involve some type of bradycardia. In first-degree AV block, no beats are skipped but the PR interval is too long. This can be normal in athletes. Second-degree AV block comes in two types. In Mobitz type I or Wenckebach phenomenon, the PR interval lengthens over a few beats until the P wave is dropped altogether. This is less likely to indicate heart disease than Mobitz II phenomenon, which involves a consent PR interval with intermittent dropping of QRS complexes in a relatively consistent pattern, such as 3:1 block or 4:1 block. This is often so symptomatic that a pacemaker is required. Figure 6 shows what a second degree Mobitz II heart block looks like:

Figure 6.

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Third-degree AV block comes from a complete absence of connection between the P waves and the QRS complexes. The ventricular rhythm you’ll see is a junctional or AV nodal escape rhythm. The rate is very slow and the symptoms are more significant than is seen with other AV blocks. The only effective treatment for this is to provide pacemaker therapy. Atropine will help but will be a short-term solution to the problem.

ANGINA PECTORIS The patient with angina pectoris generally has a predictable pattern of chest pressure or discomfort that comes on with exercise and is relieved by stress. It is often due to reversible or transient myocardial ischemia without true myocardial infarction. Stress can also bring this on. The actual problem is one of myocardial oxygen demand exceeding the blood supply from the coronary arteries. The cardiac workload is made worse by aortic stenosis, hypertension, hypertrophic cardiomyopathy, and aortic regurgitation. If there is anemia or high altitude, the problem will be made worse.

The atherosclerotic lesion of the coronary arteries may be fixed but the narrowing itself will not be fixed. There will be changes in the vascular tone so that in the morning, for example, when the tone is greater, the chances of angina symptoms are also greater.

High levels of catecholamines are causative of vasoconstriction that also contributes to the problem.

The patient with typical angina will have chest pressure of variable intensity that may radiate to the jaw, neck, shoulder, or arms. In atypical angina, the patient will have gas, bloating, or abdominal pain instead of chest pain. Most of the time, the symptoms will come on with activity and will go away with rest, which provides a clue as to the causation. Some people may have nocturnal angina if they are having vital sign changes while dreaming. Diabetics have a much higher risk of silent ischemia because of nerve damage that affects the pain experienced by the heart.

The diagnosis is made through evaluation of the symptoms, the ECG showing no evidence of ongoing ischemia at rest, and stress testing, which will show ischemia with exercise. If this test is positive, a coronary angiography can be done in order to confirm the presence of narrowing of the coronary arteries.

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The treatment for angina pectoris is multifactorial. All modifiable risk factors need to be addressed, such as the cholesterol level, high blood pressure issues, obesity, and smoking—all of which will worsen the progression of the disease. Antiplatelet drugs should be given on a regular basis, such as aspirin, ticagrelor, prasugrel, or clopidogrel.

Symptom control should be used on an intermittent basis, such as nitroglycerin or calcium channel blockers. Things that will help lessen disease progression are ACE inhibitors for blood pressure and statin drugs for hyperlipidemia. The severely affected patient might need revascularization if medical therapy fails.

HYPERLIPIDEMIA Hyperlipidemia is a major cause of cardiovascular disease, which is why all heart patients are good candidates for treatment of dyslipidemia. Remember that dyslipidemia can be related to an elevated total or LDL cholesterol, an elevated triglyceride level, or a low HDL level. Any of these will lead to atherosclerosis, which is the most common cause of the different types of heart disease. People can have primary or secondary dyslipidemia, with primary dyslipidemia being genetic in nature.

Labs will have a breakdown of what constitutes and elevated lipid situation but, in reality, there is no real cutoff involved where the risk for heart disease does not exist.

People with other risk factors require much lower levels of cholesterol compared to those who have no other risk factors. Dyslipidemias are classified by an increase in cholesterol only, an increase in triglycerides only, or increases in both cholesterol and triglyceride levels. This doesn’t take into account that their might be a low HDL situation as well.

Most primary dyslipidemias are either single gene or multiple gene mutations affecting the production or clearance of cholesterol or triglycerides. These tend to run in families.

In some cases, being a heterozygote for a single-gene disorder leads to a moderate increase in heart disease risk but being a homozygote is associated with a high risk of early heart disease.

Among secondary causes of dyslipidemia, one of the more common ones is living a sedentary lifestyle with a high calorie, high-fat diet. Other causes include chronic kidney

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disease, diabetes mellitus, hypothyroidism, primary biliary cirrhosis, cigarette smoking, HIV disease, and certain drugs that affect cholesterol.

Diabetes is one of the highest risk disorders contributing to dyslipidemia. This is because they have naturally high triglyceride levels, abnormally small LDL particles, and low HDL levels. Type 2 diabetics are higher risk than type 1 diabetics. The added issues of obesity, physical inactivity, and high caloric intake make it more likely that dyslipidemia will be present.

While dyslipidemia has not typical symptoms, having the condition means having high levels of coronary artery disease, stroke, and peripheral vascular disease. If the triglyceride level is markedly high, acute pancreatitis can occur. There will be skin changes, such as tendinous xanthomas of the Achilles tendons or over the extensor joint surfaces, eruptive xanthomas on many body areas, arcus corneae of the eyes, and xanthelasma of the eyelids. Figure 7 shows what xanthelasmas look like:

Figure 7.

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Once a person has been tested and found to have dyslipidemia, it is a good idea to evaluate their clinical picture for evidence that they have end organ damage, such as coronary artery disease, stroke, or peripheral vascular disease. All patients with elevated LDL cholesterol should have a reduction in dietary fat and cholesterol content, maintenance of ideal body weight, and a high fiber diet. Exercise seems to help in mild cases but the high risk patient should have consideration for statin drug therapy.

Statins are the main treatment of choice for dyslipidemia, largely because they are known to reduce morbidity and mortality of heart disease. There are many statin drugs that work in the same way. Other options include bile acid sequestrants that block bile acid reabsorption in the intestines, cholesterol absorption inhibitors like ezetimibe, and PCSK0 monoclonal antibody therapy. Patients with severe disease from homozygous familial hypercholesterolemia can take mipomersen or lomitapide, which block the synthesis of apo B in the liver in order to decrease the LDL cholesterol.

High triglycerides are often treated with lifestyle changes, although fibrates will reduce the triglyceride level by half. Statin drugs will also help, as will omega-3 fatty acids. Apo CIII inhibitor drugs are not available everywhere but are used in severely elevated triglyceride circumstances. Low HDL is difficult to treat and exercise is most recommended as a way to combat this problem. Nicotinic acid and fibrates may also help to a slight degree.

PERIPHERAL VASCULAR DISEASE The main cause of peripheral vascular disease is atherosclerosis of the lower legs, leading to ischemia of the toes first and then proximally over time. It is often asymptomatic with the first sign being leg or calf pain with exercise. As the disease progresses, the pain will worsen with decreasing levels of exercise and there will be findings of cyanosis, hair loss, skin atrophy, ischemic leg ulcers, and gangrene. The major cause of death is some other type of cardiovascular disease, such as stroke or heart attack. The major risk factors are hyperlipidemia, diabetes, high blood pressure, smoking, older age, diabetes, male gender, and obesity. Peripheral arterial disease is a manifestation of systemic atherosclerosis, affecting other body areas as well.

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In your diagnosis of peripheral arterial disease, you will start by getting an anklebrachial index, which is a blood pressure evaluation of the ankle and brachial arteries, dividing these two numbers. If the level is less than 0.9, the diagnosis is that of peripheral vascular disease. If further evaluation is further indicated, a Doppler ultrasound will help detect blood flow through the arteries in a noninvasive way. The gold standard is angiography or a dye study, used to detect specific areas of occlusion or narrowing, particularly before surgical intervention, if this is indicated.

The treatment of all patients requires risk factor modification to include smoking cessation, dyslipidemia treatment, management of diabetes, exercise, management of hypertension, and improved diet. Statin drugs, aspirin, and ACE inhibitors are required to slow progression. Walking is a good form of exercise so this should be undertaken.

Preventive foot inspections and foot care are also essential.

Drug therapy should include aspirin or other antiplatelet drugs like dipyridamole, clopidogrel, or ticlopidine. The claudication itself can be treated with pentoxifylline or cilostazol. If these fail to help, percutaneous transluminal angioplasty is indicated using a stent to keep the vessel open or to prevent gangrene. This works best for short or just a few lesions. If the disease is extensive, then surgical interventions, like bypass grafting or revascularization is indicated. A thromboendarterectomy can be done to remove existing clots and a sympathectomy is done to remove the sympathetic nervous system’s impact on the leg vessels. An amputation is done as a last resort if there is gangrene that cannot be fixed with other surgery.

CONGESTIVE HEART FAILURE Congestive heart failure involves some type of left ventricular or right ventricular dysfunction, leading to a backup of fluid into the lungs or peripheral tissues. It is a common disease, affecting more than six million patients in the US. There are two types of heart failure, including heart failure with preserved ejection fraction and heart failure with reduced ejection fraction.

Heart failure with preserved ejection fraction is called diastolic heart failure with an increase in end-diastolic pressure at rest or with exertion and an essentially normal

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ejection fraction. Common causes include constrictive pericarditis, valvular disease, and high levels of ventricular stiffness. It is common in older adults and is seen in hypertrophic cardiomyopathy, amyloidosis, hypertension, and aortic stenosis. Heart failure with reduced ejection fraction involves output or systolic heart failure so that the output of the heart is reduced.

If left heart failure is seen, the fluid backs up into the lungs. There is worsened symptoms with lying down and major symptoms of dyspnea that is worse at night and with exertion. The worst case scenario is pulmonary edema, which is often lifethreatening. Some patients will die of acute respiratory failure.

Right ventricular failure involves backup of fluid into the systemic venous system, leading to hepatomegaly, ascites, and peripheral edema. The stomach and intestines become congested so absorption of nutrients is poor. The patient will have diarrhea from malabsorption and protein-losing enteropathy, which worsens their outcome.

Heart failure is different from cardiomyopathy, even though cardiomyopathy can lead to heart failure. Cardiomyopathy is a disease of the myocardial cells, which are damaged for many reasons, including inflammatory diseases, ischemic heart disease, hypertension, and hypertrophy of the myocardium. It is also possible to have what’s called high-output heart failure, which is caused by things like thyrotoxicosis, beriberi, end-stage liver disease, severe anemia, prolonged tachycardia, arteriovenous fistulae, and advanced Paget disease.

The diagnosis of asthma is made by getting a clinical history and a chest x-ray to rule out lung disease and to see if there is cardiomegaly. An ECG can show if there has been a myocardial infarction or evidence of ischemia. To assess whether or not there are issues with reduced ejection fraction, an echocardiogram, MRI of the heart, or radionuclide scan of the heart can be done. The main blood test for heart failure is the BNP or brain natriuretic peptide level. An alternative is the N-terminal-pro-BNP level, which will essentially assess the same thing. It is a sensitive test but a normal BNP level does not exclude the diagnosis of heart failure. A coronary angiography or CT coronary angiography is only indicated when the probable cause is coronary artery disease.

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In treating the heart failure patient, the approach is multifactorial. Inpatient management is recommended for the patient who has severe symptoms or worsened heart failure over a brief period of time. The short-term goals are to relieve symptoms without worsening hypokalemia, hypotension, or renal dysfunction. Over the long term, the underlying cause is addressed, such as correction of hypertension, improving cardiac function, and maximizing quality of life.

Most patients need extensive education about their disease and instruction on how to avoid eating excessive amounts of salt. Sodium restriction is necessary in most cases as are lifestyle measures, such as weight loss, improved diet, and initiation of exercise.

Underlying conditions, such as hypertension, diabetes, dyslipidemia, and smoking need to be addressed.

Many patients will need some drug therapy. This includes digoxin, nitrates, and diuretics to improve symptoms acutely. Long-term management involves chronic use of ACE inhibitors, beta blockers, angiotensin II receptor blockers, aldosterone antagonists, among others. Arrhythmias are treated according to their underlying cause. This might involve normalizing electrolytes, controlling the heart rate, and using antiarrhythmic drugs. Atrial fibrillation should be managed, especially if the heart rate is too high.

The rare patient might need an implantable cardioverter-defibrillator or ICD or possibly a cardiac resynchronization therapy or CRT. The ICD will restart the heart spontaneously if the person develops an unsustainable rhythm, while CRT is another implantable device that also has an ICD component. These are expensive devices but will improve heart function and reduce death rates due to heart failure complications.

LV assist devices are also implantable but will help augment the left ventricular output as a bridge to receiving a heart transplant if this is necessary.

The main surgical options include coronary artery bypass grafting if ischemia underlies the problem. If the person has valvular disease as a cause of their heart failure, the valve needs to be replaced or repaired. The end-stage treatment for those under sixty years with severe heart failure is to recommend a heart transplant, which will prolong life for up to 10 or more years.

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AORTIC DISSECTION An aortic dissection is a life-threatening emergency in which there is a tear in the intima of the aorta so that the intima and media separate. This creates a false lumen through this area where blood passes. This can happen anywhere along the length of the aort and will extend to involve other arteries above and below the dissected area. This is a more common complication among the elderly, black people, and those with hypertension.

Those with a connective tissue disorder, such as Marfan syndrome or Ehlers-Danlos syndrome have a greater chance of having this complication as well.

There are different ways to classify an aortic dissection, usually according to anatomic location. The most widely-used classification system is the DeBakey system, which classifies dissections by where they are located. About half of all dissections start in the ascending aorta and reach up to the aortic arch. They tend to occur where the greatest amount of hydraulic stress is found, such as the first five centimeters of the ascending aorta on the right lateral wall as well as on the proximal descending aorta past the left subclavian artery.

A dissection rarely happens if the aorta is normal. In situations where there is a connective tissue disease, hypertension, or atherosclerosis, the aortic wall is already damaged and a dissection is more likely to occur. The consequences are great, including compromise of nearby arteries, aortic valve regurgitation, heart failure, and aortic rupture.

The patient with an acute aortic dissection will describe the abrupt onset of tearing or ripping pain in the upper chest or back. About one-fifth of patients have syncope for a variety of reasons, including active bleeding or severe pain with syncope. If perfusion of major organs is involved, there can be symptoms related to intestinal infarction, myocardial infarction, and stroke, among other complications). The major pulses might be interrupted or limb pulses might differ from side to side. Half will have an acute aortic regurgitation murmur. Arterial supply to any major branch of the aorta can be obstructed.

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The diagnosis of aortic dissection is made through several options. A transesophageal echocardiogram, CT angiography, or magnetic resonance angiography can be used to make the diagnosis in situations where the patient has symptoms of this problem. The tests will show an intimal flap as well as a double lumen in the aorta. If surgery is considered, a contrast aortography is recommended to specifically outline the limits of the problem. While an ECG will show abnormalities, these will not be diagnostic of the problem.

About 20 percent of affected patients will die immediately before reaching a medical facility. At 1 year, about 90 percent will ultimately die of some type of complication of their dissection. The goal of medical management is to decrease the arterial pressure, the shear stress on the artery, the contractility of the ventricles, and the patient’s pain.

Beta-blockers are a first-line treatment for blood pressure control. Other choices include calcium channel blockers or nitroprusside, although nitroprusside cannot be used alone because of reflex sympathetic activation.

Ultimately, the patient will require surgical repair of their dissection unless the problem is uncomplicated and part of the descending aorta alone. Surgery is designed to remove the false channel and provide a graft through which blood can flow. Open or closed repair can be done to achieve these goals. The surgery is often complicated by stroke, paraplegia, renal failure, or death.

VALVULAR HEART DISEASE Heart valve disorders involve either stenosis or regurgitation. Stenosis is narrowing of the outflow of the valve, while regurgitation is leakage backward of blood through the valve. Any valve of the heart can be both regurgitant and stenotic. The mitral valve might be neither but will be involved in mitral valve prolapse, in which the valve leaflets billow back but usually not enough to cause leakage of the valve itself.

A valvular disorder can be diagnosed though observation and auscultation, which can lead you to determine that a problem exists. An actual diagnosis, however, is gotten through cardiac ultrasound, such as a standard 2D ultrasound, which will show the anatomy of the valves. An ECG will detect the heart rhythm and electrical abnormalities,

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a chest x-ray will detect pulmonary congestion and heart size, while a Doppler ultrasound will evaluate the pressures inside the heart.

Most of the time, mild valvular disorders can be managed symptomatically until it becomes necessary to replace or repair the valve. A valvuloplasty is a valve repair surgery, while valve replacement can involve an artificial valve or a porcine, pig-derived or bovine, cow-derived valves. Those with valvular disease often require antibiotic prophylaxis to prevent bacterial vegetations from developing during certain surgical or dental procedures.

Patients with a prosthetic valve will require long-term anticoagulation therapy, especially if the person has a mechanical valve. The target IRN should be quite high in order to avoid thromboemboli from occurring. The only accepted anticoagulant for those who have prosthetic valves is warfarin. The newer anticoagulants are insufficient, although heparin can be used if warfarin is not recommended, such as with a pregnant patient. Patients who also have stents will require aspirin, clopidogrel, and warfarin at the same time.

PERICARDITIS Pericarditis represents an inflammation of the pericardium, usually with accumulation of fluid in the pericardial sac. The inflammation can be due to infection, trauma, myocardial infarction, cancer, or metabolic disease. The patient will have pain or tightness in their chest, worse with deep inspiration. If there is constriction or decreased cardiac output associated with this, there will be symptoms of cardiac tamponade.

Remember that the pericardium has two layers: the visceral layer attached to the myocardium and the parietal layer covering the heart. The pericardial sac contains a very small amount of fluid under normal circumstances. These layers are stretchsensitive so it doesn’t take much extra fluid to cause increased pain.

Pericarditis may be acute, subacute, or chronic. Acute pericarditis develops quickly and often leads to a pericardial effusion and secondary inflammation of the outer myocardial layers. Subacute pericarditis comes on within weeks to months and can be an extension of acute disease. Chronic pericarditis happens after six months of inflammation. The 24

fluid that builds up can be chyle, pus, blood, serous, or serosanguineous in nature. If cardiac tamponade happens, the cardiac output will drop and fluid backs up, and shock can occur. Symptoms will be less if the fluid buildup happens slowly versus when it comes more quickly.

Constrictive pericarditis is not common but comes when the pericardium is fibrotic and thick. Calcium deposits and scar tissue between the layers can complicate the picture. It is more common for these to lead to rhythm disturbances than to fluid accumulation.

The problem is that the cardiac output drops so much that there will be an elevation of venous pressures, hepatic congestion, and cirrhosis from this congestion.

Most cases of acute pericarditis are inflammatory from radiation, drugs, uremia, myocardial infarction, infection, or autoimmune disease. Most infectious cases are viral or cannot be identified at all. Post-MI pericarditis is called Dressler syndrome, which is now less commonly seen.

Chronic pericarditis can also have the same etiologies as acute and subacute pericarditis, although cholesterol pericarditis and hypothyroidism can also be causative of the symptoms. Another common cause of chronic pericarditis is some type of metastatic cancer.

Most acute pericarditis patients will have significant pain and an obvious pericardial friction rub. Some will be short of breath. If there is tamponade, you can expect hypotension, pulmonary edema, jugular venous distension, and other evidence of venous congestion. The pain may be similar to an MI because of the similarities in their innervation but inspiration and swallowing may exacerbate the symptoms. If the cause is inflammatory or infection, the patient may have fever, chills, and cough.

Chronic pericarditis and constrictive pericarditis do not always have the same symptoms but, if the cardiac output is impaired, the major finding will be of peripheral venous congestion, such as hepatomegaly, jugular venous distension, and peripheral edema. An echocardiogram and ECG plus a chest x-ray will help identify a pericardial effusion but won’t identify tamponade because large volumes of up to 1500 milliliters of fluid will be tolerated if the buildup is gradual. Cardiac tamponade is a clinical and not an imaging diagnosis.

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A serial ECG may show evidence of pericarditis. There will often be classic upward concave elevations of the ST segment, which are seen in Figure 8:

Figure 8.

In looking for a cause of the pericarditis, it is not necessary to do much in a healthy young person who likely has idiopathic or viral disease. Other testing done if necessary include a diagnostic pericardiocentesis or a pericardial biopsy, looking for things like tuberculosis, cancer, or bacterial infection. Besides a culture and cytology of the fluid, other tests of the fluid are nonspecific and not helpful in making the diagnosis. There are blood tests for autoimmune disease, acute-phase reactants, HIV disease, viral antibodies, and a CBC that can be done.

When treating these patients, those with severe features need hospitalization. Stop all possible causative drugs and do a pericardiocentesis if this is causing symptoms. A pericardiocentesis without an echocardiogram to guide the procedure can be lethal so it should wait until it can be done under guidance. Colchicine or aspirin can be used for pain and prednisone for a week will help if the colchicine or aspirin do not help. In refractory disease, triamcinolone can be injected into the pericardial space. Severe constrictive pericarditis is treated surgically with resection of the pericardial sac but the mortality rate of the procedure itself is high.

ENDOCARDITIS Endocarditis can be due to several things but most are infectious and most infections are due to staph or strep infections. Fungal infections can also cause this problem.

Expect to see fever, petechiae, heart murmurs, embolic diseases, anemia, and an imaging study showing endocardial vegetations on the heart valves. In noninfective 26

cases, there will be platelets and fibrin strands on the valves, but these will be sterile.

The diagnosis is mostly clinical but can be confirmed with imaging.

Predisposing factors to developing this problem include heart valve diseases, hypertrophic cardiomyopathy, or prior endocarditis. Those with structural congenital heart diseases have an increased risk of endocarditis as well. The organisms involves usually come from distant sites, such as the mouth, cutaneous abscesses, or known portals of entry through the skin. Pacemakers and shunts can also be sources of infection. Most infections are from staph or strep but other bacteria and fungi can cause this problem.

The three stages of the infection are bacteremia, adhesion of organisms, and colonization of the adherent organisms. Many species make biofilms that protect them from host immune defenses and antibiotic therapy. The local effects include myocardial abscess formation, aortitis, and sudden valvular regurgitation leading to death. Systemic complications include all types of infectious emboli and activation of the immune system in chronic disease states.

The symptoms may vary by type of endocarditis. In subacute bacterial endocarditis, the patient will have a fever, fatigue, night sweats, weight loss, and malaise. Almost all patients will have a murmur eventually. Look for evidence of emboli to the retina, conjunctivae, skin, kidneys, or CNS. If the disease is acute, the patient will have similar symptoms but a more rapid course and the presence of toxic shock in some settings.

Right-sided disease will lead to pulmonary emboli, with symptoms of cough, chest pain, and hemoptysis.

The diagnosis is largely clinical and involves insidious symptoms but, if things like a murmur are present, this will help to make the diagnosis. Blood cultures might identify the organism but a negative culture does not rule out the disease process.

Echocardiography will often show the vegetations on the heart valves. Those with a fever who are not taking antibiotics will have a high rate of positive blood cultures, although some may need repeated cultures to get a positive one. A transesophageal echocardiogram is the best test for this but a CT scan will better show abscesses near the valves.

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Infectious endocarditis needs to be treated because it is fatal if not treated. IV antibiotics over a long course is recommended, although some patients will need valvular debridement, valve repair, or valve replacement. All patients need to be examined for a source of infection, particularly a dental source and those who have catheters or devices as causes of infection need to have these removed.

The patient who is high risk for endocarditis should have prevention of this problem. If the person is having heart valve surgery, they need preventive tooth extractions, enhanced dental hygiene, and enhanced cutaneous hygiene. Antimicrobial prophylaxis is recommended for those with prosthetic heart valves, heart transplants, or congenital heart disease. Dental procedures that involve the gingiva, respiratory tract procedures, and vaginal deliveries are all indications for prophylaxis, while known surgery involving an established infections also require prophylaxis against staph and strep infections.

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KEY TAKEAWAYS •

The patient with an acute coronary syndrome can have unstable angina, a nonST-segment myocardial infarction, or a transmural, ST-segment elevation myocardial infarction.

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The patient with an arrhythmia can be divided into an irregular or regular rhythm with a narrow or wide-complex QRS.

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The patient with atrial fibrillation needs anticoagulant therapy in order to prevent thromboembolic disease.

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Angina is generally a chronic heart condition that itself is a risk factor for a myocardial infarction.

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Dyslipidemia can be primary or secondary but is generally treated the same way, according to the type of dyslipidemia they have.

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Peripheral vascular disease leads to claudication and is a marker for more diffuse cardiovascular disease.

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Heart failure is divided into those cases with preserved ejection fraction and those with reduced ejection fraction.

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Aortic dissection usually involves the ascending aorta and can affect vessels coming off the aorta itself.

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Pericarditis is due to a variety of conditions and may include a pericardial effusion that causes cardiac tamponade.

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Endocarditis is usually fatal without treatment and involves bacterial or fungal infections of the valves of the heart.

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